Published online Mar 25, 2025. doi: 10.5501/wjv.v14.i1.100489
Revised: October 1, 2024
Accepted: October 28, 2024
Published online: March 25, 2025
Processing time: 102 Days and 1.1 Hours
Arboviral diseases are viral infections transmitted to humans through the bites of arthropods, such as mosquitoes, often causing a variety of pathologies associated with high levels of morbidity and mortality. Over the past decades, these in
Core Tip: This review delves into the historical characteristics, pathogenesis, and clinical management of the four major arboviruses that have triggered outbreaks worldwide: Dengue, Zika, yellow fever, and chikungunya fever. It aims to elucidate the viral characteristics, cellular tropism, and immune evasion mechanisms, as well as the primary clinical manifestations and their complications, laboratory diagnosis, treatment, prevention, and vaccines either currently available or under development. Thus, with a focus on the medical and scientific fields, this review enables the reader to acquire comprehensive and generalized knowledge about each of these arboviruses.
- Citation: Cenci Dietrich V, Costa JMC, Oliveira MMGL, Aguiar CEO, Silva LGO, Luz MS, Lemos FFB, de Melo FF. Pathogenesis and clinical management of arboviral diseases. World J Virol 2025; 14(1): 100489
- URL: https://www.wjgnet.com/2220-3249/full/v14/i1/100489.htm
- DOI: https://dx.doi.org/10.5501/wjv.v14.i1.100489
Arboviruses are an extensive group of viruses that have arthropods (insects and arachnids) as their primary vectors, transmitting the viruses to vertebrate hosts, such as humans, through their bites along with their saliva[1]. These infections are endemic to tropical and subtropical regions, where approximately 3.9 billion people live today, disproportionately affecting the poorest populations[2]. However, with rising temperatures due to global warming, there is a greater spread of the main urban vectors of arboviruses worldwide, such as mosquitoes of the genus Aedes [Aedes aegypti
Currently, the main arboviruses with the potential to cause worldwide outbreaks are the dengue virus (DENV), with an estimated 96 million symptomatic cases and 40000 annual deaths in more than 129 countries[2], in addition to the Zika virus (ZIKV), the yellow fever (YFV) virus, and the chikungunya (CHIKV) virus (viruses which also have the capacity to generate morbidity and mortality). All these diseases have epidemic potential, as evidenced by their significant global outbreaks in the last decades[7,8].
According to the World Health Organization (WHO), arboviruses are responsible for 17% of all infectious diseases and cause approximately 700000 deaths annually worldwide[2], directly affecting the healthcare systems of developing and even developed countries. These diseases can overcrowd hospitals during outbreak periods and cause chronic complications in infected patients, leading to increased healthcare costs and considerable social damages. These impacts are further exacerbated by the limited knowledge about the viral characteristics and the suitable clinical management. Thus, this article aims to elucidate the pathogenic mechanisms of each of the four main arboviruses, with the intention of understanding aspects related to viral characteristics, tropism, immune response, and viral evasion, as well as the main symptoms, possible complications, treatment, vaccines, and prevention, highlighting the main points of appropriate patients’ clinical management.
DENV is a positive-sense single-stranded RNA virus that belongs to the Flavivirus genus within the Flaviviridae family. There are four known serotypes spread globally: DENV-1, DENV-2, DENV-3, and DENV-4. Its RNA encodes 10 proteins, including three structural: Capsid (C), membrane (prM/M), and envelope (E); and seven non-structural, associated with RNA replication: NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5[9,10].
DENV is primarily transmitted by Ae. aegypti and Ae. albopictus mosquitoes[11]. Initially, Ae. aegypti was thought to be the sole vector capable of causing significant outbreaks. However, recent research indicates that Ae. albopictus also plays a significant role in sustaining large outbreaks and has contributed to the resurgence of DENV, particularly in Southeast Asia[12]. Dengue fever, caused by DENV infection, is considered the most important mosquito-borne viral disease, spread globally[13], with 50-100 million people infected yearly[14]. Dengue incidence has started to notoriously increase since 1990[15], and numerous social and economic factors might explain this phenomenon[9], as well as global warming, seeing that it can contribute to the re-emergence of DENV by expanding the geographical range of mosquitoes and increasing infection rates[16].
Although most dengue cases present as mild or asymptomatic (anorexia, retro-orbital pain, myalgia and rash), approximately 5% progress to a more severe form[17], primarily attributed to immunological factors such as the cytokine storm and antibody-dependent enhancement[18], that cause an exacerbation of the inflammatory process, leading to increased vascular permeability and a risk for hemorrhage and shock[19], usually followed by persisting vomiting and abdominal pain, as well as other various warning signs[20]. Such severe cases are mostly seen in heterotypic secondary infections (infection with a different serotype) but can also occur primarily in children who inherit immunity from their mothers[21] correlating with an impaired adaptative immune response. Even though hard to predict, certain authors argue that elevated viremia is correlated with severity[22], while others refute this idea[23], and instead propose evaluating factors like viral NS1 protein levels or host cytokine expression[24].
This complex host-pathogen interaction occurs within the context of the DENV’s cyclical transmission process, involving human-mosquito and mosquito-human transmission. It is not very easy to predict sporadic outbreaks, as around 80% of DENV transmission occurs via asymptomatic hosts[25]. In this process, healthy mosquitoes acquire the virus by feeding on the blood of an infected host, and once the virus has infiltrated the vector’s tissues, it becomes infected for life, and capable of transmitting the virus[26]. When an infected vector feeds on a naive host’s blood, mos
Viral entry, replication, and release: Upon injection into the skin, cells of the monocyte lineage, such as macrophages, Langerhans cells and dendritic cells are among the primary targets[27]. Other potential targets include endothelial and epithelial cells, lymphocytes, hepatocytes, fibroblasts and keratinocytes[28] with reports of viral presence in various tissues, including the dermis (skin), blood, bone marrow, lymph nodes, liver and occasionally, the brain[29]. Cellular internalization of DENV occurs through envelope protein (E) interaction with numerous different receptors, including heparan sulfate proteoglycans[30], DC-Sing[31], heat shock protein (HSP) 70 and HSP90[32], triggering receptor-mediated endocytosis, that can be dependent or independent of clathrin. Fc and C1q receptors can also facilitate entry via antibody-mediated pathway[33]. Additionally, alternative entry pathways such as diffusion and macropinocytosis have been reported. The specific entry route for DENV also varies depending on the virus serotype[34,35].
Subsequently, the virus’s E protein undergoes irreversible conformational changes due to the endosome’s low pH, leading to fusion with the endosomal membrane[36], facilitated by hydrophobic peptides[36,37]. Following its release, the viral genome acts as a mRNA and gets translated into a single polypeptide, later processed and cleaved by host and viral proteases, resulting in the ten viral proteins. The seven non-structural proteins form a replication complex through in
During this process, numerous viral mechanisms have been observed to take place in order to maximize replication, including reprogramming protein synthesis in host cells to favor viral RNA translation[41], regulating cellular apoptosis through interaction between NS5 protein and the mechanistic target of rapamycin complex 2[42], binding between NS1 and Beclin 1[43], and maximizing ATP production by promoting anaerobic glycolysis via the hypoxic response[44] or activating lipophagy to enhance β-oxidation[45].
Once enough proteins are synthesized and the virion is assembled, it is again processed by the Golgi apparatus changing its surface from spiky to smooth[9,46]. Then, mature virions are secreted from the infected cell along with NS1 hexamers, that play a crucial role in the disease pathogenesis and severity[47].
Innate response and evasion: The innate immune response to DENV initiates upon the first cell infection and progresses concurrently with viral replication and release, rather than following these events[48]. Not surprisingly, the virus has developed multiple strategies to evade the host’s innate response, primarily through its non-structural proteins[49].
When a dengue virion infects its initial target host cells, it activates pattern recognition receptors (PRRs) such as retinoic acid-inducible gene 1 (RIG1), melanoma differentiation-associated protein 5 (MDA5), toll-like receptor 3 (TLR-3), and TLR-7[50]. This sets off the signaling cascade of the innate response, leading to the release of cytokines and ultimately resulting in the expression of type I and III interferons (IFNs), recruitment of additional monocytes, and activation of the complement system[49]. Meanwhile, infected dendritic and Langerhans cells migrate to the lymph nodes and present viral antigens, initiating the adaptive response[51]. If successful, the antiviral response will counteract viral replication and infection. However, DENV evades it through its non-structural proteins (NS1 to NS5), which can disrupt receptor signaling, IFN synthesis, and regulation pathways[52-55]. Additionally, DENV’s NS1 protein can inhibit the complement response by interacting with its protein complexes[56].
In a more passive way, DENV evades the immune response by forming the replication complex, that serves as a “barrier”[40], and by regulating cellular apoptosis, a common mechanism used by the immune system to suppress viral replication[57]. Furthermore, DENV’s capability of infecting defense cells is itself a mean of dysregulating the host’s antiviral response.
Despite its notable role in dengue pathogenesis, the innate response is not typically singled out as a factor in dengue severity, whereas the adaptive immune response has been pointed as the primary contributor, due to impaired immune responses against different serotypes[58].
Adaptative response and antibody-dependent enhancement: The adaptive immune response to DENV begins with antigen-presenting cells (APCs) presenting viral antigens to T cells in lymph nodes. This activation leads to differentiation of T lymphocytes into effector and memory T cells, providing long-term immunity against infections with the same serotype, but only short-term immunity against heterotypic infections[59]. DENV has shown capability of interacting with numerous factors regarding antigen-specific immunity, such as priming and activation of T and B cells[60], antibody production and neutralization properties, along with cytokine release[61]. The highlighted factors have a significant impact on the disease pathogenesis and will be further discussed.
DENV is able to impair T lymphocyte priming and activation either by antigenic variation or inducing apoptosis of APCs[62]. This leads to a compromised T cell response, regarding both CD8+ direct targeting of infected cells and CD4+ differentiation into helper T cells, the ladder being related to activation of B cells and antibody production. Anti-DENV neutralizing antibodies primarily target specific regions of the E and C proteins[63,64], and can also target the NS pro
Antibody-dependent enhancement occurs when antibodies bind to the virus but fail to neutralize it, forming an antibody-virus complex[67]. This phenomenon is exacerbated by the original antigenic sin, where antibodies from the primary infection are more prevalent than those from the secondary infection. The antibody-virus complex can more efficiently enter monocytes by interacting with Fc and C1q receptors and triggering endocytosis, enhancing viral re
Recent studies have also demonstrated the potentiality of autoimmunity in dengue pathogenesis. Anti-NS1 antibodies can interact with endothelial cells (ECs), triggering inflammatory cytokine signaling and cellular apoptosis[72], and autoantibodies targeting ECs and platelets have also been observed, correlating to the increased vascular permeability seen in secondary dengue infections[73,74].
Overall, the adaptive immune response is a significant factor in dengue severity during secondary infections, especially regarding the process of antibody-dependent enhancement. These events, related to the evasion of the adaptive response, ultimately result in increased inflammatory process and vascular permeability, which are the main causes of dengue severity.
Cytokine storm and vascular permeability: Cytokine release is a common physiological event in the immunological system[75]; however, the exacerbated release of cytokines is one of the main events in severe cases of dengue. It is mostly observed in secondary infections[76], correlating with the impairment of the immune response. The molecular mecha
Events of the cytokine storm can be triggered by viral infection of both leukocytes and ECs[77], but also by the interaction of the NS1 protein with receptors such as TLR-4[78,79]. High levels of cytokines such as interleukin 1 (IL-1), IL-4, IL-8, IL-10, IL-13, and IL-17, as well as C-X-C motif chemokine ligand 10 (CXCL10), tumor necrosis factor-alpha (TNF-α), vascular endothelium growth factor A (VEGFA), macrophage migration inhibiting factor (MIF), IFN-β, and IFN-γ have largely associated with disease severity[61,80]. These cytokines are closely related to the increase of vascular permeability and subsequent plasma leak, and also to disrupting tight junctions[81] and inducing autophagy[82], with in vitro studies suggesting more specific roles of different cytokines, such as MIF’s role in EC glycocalyx degradation[83,84] and the roles of CXCL10, VEGFA, and TNF-α in increased permeability and EC apoptosis[80,85,86]. For instance, a recent longitudinal study conducted by Bhatt et al[87] suggests that the analysis of cytokine levels in patients can be useful in predicting dengue severity.
Interestingly, anti-inflammatory cytokines such as IL-4 and IL-10 have been shown to paradoxically contribute to more inflammation, as they can suppress the immune response and impair viral clearance, increasing viral dissemination[88]. Moreover, cytokines that recruit more leukocytes to the site of inflammation, such as IL-8, IFN-γ, MIF, TNF-α, and CXCL10, can contribute to more infection and viral replication, since DENV has a tropism for these types of cells[89].
In summary, the cytokine storm is amplified during DENV infection due to a process of positive feedback, in which the release of cytokines and recruiting of leukocytes leads to even more inflammation. This ultimately results in events of vascular leak, which are maintained and amplified by DENV-induced coagulopathy and thrombocytopenia[90].
Coagulopathy and thrombocytopenia: Besides inducing vascular leak through endothelial damage and a cytokine storm, DENV employs numerous mechanisms to disrupt coagulation, which is meant to contain plasma leakage. Such events can occur via activating and dysregulating coagulation pathways, and also impairing various steps of the coagulation process[91].
In vitro and in vivo studies have demonstrated multiple ways DENV induces coagulopathy and thrombocytopenia. In bone marrow, the virus has been shown to suppress its activity and interfere with megakaryocyte maturation, either directly through infection and interaction with E protein[92] or indirectly via cytokines[93]. Apart from affecting megakaryopoiesis, early activation through DENV NS1 binding to TLR-4 on platelets can potentially cause apoptosis[79], platelet phagocytosis by macrophages and dysregulated clot formation[94], leading to platelet ‘waste’ and thrombocytopenia. DENV infection can also promote the production of cross-reactive antibodies that target platelets[95] and coagulation factors such as thrombin and plasminogen[73], resulting in imbalanced coagulation and fibrinolysis, ultimately leading to amplified vascular permeability. A simplified schematic representation of the discussed immunological aspects of dengue pathogenesis can be seen in Figure 1.
All of the highlighted aspects act dynamically and synergetically, ultimately resulting in increased vascular leak and risk for hemorrhage, correlating with dengue’s clinical manifestations and major complications.
Clinical manifestations: Most cases of dengue infection are asymptomatic, but some patients can manifest symptoms after an incubation period of 3-15 days. Traditionally, dengue was classified into the stages of dengue fever (DF), dengue hemorrhagic fever, and dengue shock syndrome (DSS)[96], with plasma leakage identified as the main factor to disease severity[97]. However, in 2009, the WHO published an update, categorizing the disease as “dengue without warning signs” (DWS-), “dengue with warning signs” (DWS+), and “severe dengue” (SD), aiming to improve on the limitations of the previous classification and broaden the assessment and management of warning signs. Unusual manifestations and involvement of various body systems beyond typical dengue symptoms are categorized under “extended dengue” (ED)[98]. Due to its importance and recent resurgence, the specific guidelines for dengue identifying and management have been reinforced worldwide, with the publishing of management manuals by important health organs.
Dengue presents dynamically with an abrupt onset of symptoms. It starts with a febrile phase, usually exceeding 38 °C[99] and lasting for 2-7 days, followed by symptoms such as anorexia, retro-orbital pain, myalgia, arthralgia, diarrhea, nausea, vomiting[100] and a maculopapular rash in 50% of cases, spreading from the face to the limbs[99]. The early phase of the disease can be nonspecific and challenging to differentiate from other febrile illnesses, especially arboviral diseases. In such cases, if the epidemiological factors are compatible, dengue management measures are recommended even if laboratory diagnosis has not been obtained, due to its potential for severe complications[99,101].
Most patients experience defervescence and recover within 3-7 days[100]. However, some patients may progress to a critical phase following fever reduction, characterized by increased plasma leakage. Symptoms can include abdominal pain, persistent vomiting, lethargy, bleeding tendencies, and fluid accumulation in the lungs (pleural effusion) or abdominal cavity (ascites) as well as disseminated intravascular coagulation[100]. Laboratory findings during this stage typically reveal an increase in hematocrit, thrombocytopenia, and leukopenia[102]. The critical phase usually lasts about 48 hours, with peak vascular leakage occurring approximately 24 hours after onset. Said vascular leak can lead to a hypovolemic shock, causing metabolic acidosis and multisystemic impairment, potentially fatal within only 24 hours or less, if left untreated[98,99].
Patients in use of non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or aspirin may present instances of hemorrhage that are not directly related to thrombocytopenia[99], but to reduced thromboxane A2 synthesis via cyclooxygenase-1 inhibition[103]. Furthermore, ED presentations may include neurological, cardiac, and renal inflammation and dysfunction, that may present as encephalitis[104] myocarditis[105,106] and acute kidney failure[107]. Such complications have been documented in literature and require careful analysis and more specific interventions, although less common[108,109].
As of the listed symptoms, abdominal pain, persistent vomiting (three occurrences per hour or four occurrences in six hours), and mucosal bleeding are categorized as warning signs for DWS+, along with lethargy or restlessness, hepatomegaly (greater than 2 cm below the costal margin), increased hematocrit (observed in two consecutive measurements), and a decrease in platelet count (below 100000 cells/mm³)[98,110]. These signs indicate a higher risk of developing severe dengue and necessitate careful monitoring.
If the patient survives the critical phase, the recovery is characterized by gradual improvement in well-being, return of appetite, fluid reabsorption, and hemodynamic stabilization. Additionally, hematocrit levels decrease and white blood cell count will increase, in a returning to a normal state. However, it is important to note that DSS can also promote these hematological manifestations as a stress response[98], therefore, a careful analysis of these variables, alongside other clinical presentations, is crucial. Nonetheless, it is not unusual for recovering patients to present bradycardia, pruritus, polyuria, and islands of pallid areas in between the rash, indicating vascular recovery[98,99].
Diagnosis: Dengue diagnosis is crucial for decision-making in the management of suspected patients. It should be conducted carefully, considering the particularities of each specific case and context. In endemic areas, diagnosis can be based solely on clinical findings and the epidemiological context, not always requiring laboratory testing[99]. However, specific testing is also a very important tool in diagnosis, especially in cases with warning signs.
If a patient is suspected of dengue infection, tracking potential exposure by evaluating the presence of infected family members and recent travelling to endemic areas is crucial[98,99]. Vital signs, level of consciousness, and hemodynamic state must be assessed, as well as noting the presence of the most common dengue symptoms, discussed earlier (see “Clinical Manifestations”). A positive tourniquet test, along with other symptoms, suggests dengue infection, although it can yield negative results in obese patients or those already in shock, and should not be the only diagnostic tool[99,111]. All these factors should be paired with analysis of complementary laboratory findings, paying special attention to leukopenia, which has been shown to accurately indicate dengue infection[112]. It is extremely important to monitor for warning signs in newly admitted patients to promptly manage complications.
When specific testing is needed, the current stage of the disease and available resources should be considered. Up to 5 days from symptom onset, reverse transcription-polymerase chain reaction (RT-PCR) can be used, but as of requiring specialized work, it is usually not the first option[113]. Given that the acute viremic phase is sometimes missed because patients may seek medical assistance only after symptoms worsen[114], detection of NS1 antigen and IgM antibodies using enzyme-linked immunosorbent assay (ELISA), immunochromatographic assay or rapid diagnostic test kits can be useful. NS1 antigen levels are present from the beginning and typically peak around 6-10 days after disease onset[115], while IgM antibodies begin to rise after 6-14 days. These tests are simpler and provide quicker results, although they may cross-react with other flaviviruses[116]. In secondary infections, NS1 detection shows limited sensitivity[117], and IgM testing is complicated due to rapid IgG rise[114]. Distinguishing between primary and secondary infections is crucial not only for diagnostic purposes but also due to the risk of developing a more severe disease.
Therefore, detection of viral genome by RT-PCR is mostly recommended up until the first 5 days of symptoms, whereas detecting NS1 antigen and IgM antibodies with ELISA can be more effective for patients that have exceeded this mark, with higher serological levels at around 6-10 and 6-14 days, respectively[115-117]. Additionally, if a secondary infection is suspected, IgM and IgG detection can be conducted concomitantly for more specific results[116]. For every case, it is always important to pair laboratory findings with clinical and epidemiological factors in order to reassure the diagnosis.
Besides the most commonly used in clinical practice, the plaque reduction neutralization test (PRNT) is considered the gold standard for identifying DENV antibodies, seeing it is highly specific and can distinguish serotypes. However, it is not routinely used for clinical purposes, as it requires samples from both the febrile and convalescent phases with a minimum interval of 14 days, as well as specialized materials and professionals[99,118]. It is primarily used for research and surveillance purposes.
Treatment: Currently, there is no antiviral drug available for dengue, so disease treatment focuses on symptomatic control and managing complications. Patients can be categorized into groups for more specific management decisions based on their disease status, although specific guidelines for categorization may vary. The WHO categorizes patients as follows: DWS- (Group A); DWS+ and DF with co-existing risk factors or important social circumstances (Group B); and severe dengue (Group C)[98]. In contrast, the Brazilian dengue management manual categorizes patients as: Absence of warning signs (Group A); absence of warning signs but with spontaneous bleeding (Group B); presence of warning signs and/or risk factors (Group C); and presence of signs of shock, severe bleeding or organ disfunction (Group D)[99]. The Brazilian manual also emphasizes that a suspected case is enough for taking the according measurements, even if laboratory testing has not yet been done[99]. Although not always equal, the division into groups is important in order to optimize the use of hospital beds, especially in the context of large regional outbreaks, as well as how to specifically manage the disease complications. Even then, an individualized analysis to each context is important.
Patients without warning signs can be sent home, prescribed oral hydration, and advised to seek the nearest hospital if any warning signs appear. Paracetamol (acetaminophen) is usually the preferred drug for pain and fever control[98], though metamizole is also widely used in Latin American countries[99,119]. NSAIDs are not recommended, as they can increase the risk of internal bleeding and Reye’s syndrome[100].
When warning signs are present and patients are hospitalized, intravenous fluid replacement is important to prevent further complications. If shock occurs, fluid resuscitation is necessary. Crystalloid solutions are primarily used, but if shock persists and progresses to a hypotensive state, a colloid solution may be required[98,99]. Careful attention to fluid administration is crucial, as fluid overload can cause or exacerbate complications. For that, laboratory indicators should be closely monitored, and IV fluid therapy should not exceed 48 hours[99,120].
There is a lack of consensus and clear evidence about some therapeutic measurements for dengue disease. Prophylactic platelet transfusion, for example, is sometimes conducted, but some procedures seem to be inappropriate[121]. Randomized trials and observational studies have shown that there is no evidence of prophylactic transfusion in bleeding prevention[122], and that unnecessary transfusions can be harmful[122]. Still in regard to bleeding, the WHO emphasizes that patients in use of anticoagulant therapy have a higher risk of severe hemorrhage[98], but no clear instructions are given to manage this situation. Temporary suspending of these medications by specific evaluation of clinicians appears to be safe, but more studies are needed to further specify this action[123].
Due to the immunological aspects of dengue, the idea of using corticosteroids to prevent severe cases pops to mind. These drugs could supposedly be useful in the intermediate phase of the disease, seeing that is when the immune system plays the bigger role in the pathogenesis[124]. However, there is no indication for the use of corticosteroids, as most studies conducted present inconclusive results or low-quality evidence[125]. All the discussed aspects highlight the importance of a careful and individualized analysis of each patient and case, even when following specific guidelines, as it is very hard to make general affirmations[124].
The development of drugs that target dengue structural and non-structural proteins emerges as a possibility for controlling viral entry and replication in hosts. Several in vitro and in silico studies have shown potentiality in this activity[126] but it is still hard to further correlate with clinical practice, as the available animal models for testing lack a mirroring to disease severity as seen in humans[127,128]. Targeting host cellular receptors that facilitate viral entry is also a possibility, but cytotoxicity should be taken into consideration, as these receptors also serve a purpose to the host[129].
Prevention: Various prevention methods have been implied as an attempt of controlling DENV vectors, encompassing biological, chemical and environmental techniques[130]. However, they present some serious issues that impair their capacity of controlling the disease transmission.
The releasing of mosquitoes infected with Wolbachia, as well as the sterile insect technique was believed to be an effective way of vector control for Ae. aegypti and Ae. albopictus, but further analysis revealed that by eliminating larvae competition, they could increase rates of surviving adults[131]. Trying to eliminate reproduction sites and using pe
Vaccines: The development of vaccines for dengue is specially difficulted due to the phenomenon of antibody-dependent enhancement[58]. Several different types, such as live attenuated, inactive virus, viral vector and DNA vaccines are now in development[134], but only live-attenuated vaccines have made into phase III trials, as registered in the Cli
| Vaccine | Intervention/treatment | ClinicalTrials.gov ID | Status | Sponsor |
| DengVaxia© | CYD tetravalent dengue vaccine/human papillomavirus quadrivalent vaccine | NCT02993757 | Completed | Sanofi Pasteur |
| CYD tetravalent dengue vaccine/human papillomavirus bivalent vaccine | NCT02979535 | Completed | Sanofi Pasteur | |
| CYD tetravalent dengue vaccine/yellow fever vaccine | NCT01436396 | Completed | Sanofi Pasteur | |
| CYD tetravalent dengue vaccine/pentaxim™ vaccine | NCT01411241 | Completed | Sanofi Pasteur | |
| Placebo/CYD tetravalent dengue vaccine | NCT01374516 | Completed | Sanofi Pasteur | |
| Placebo/CYD tetravalent dengue vaccine | NCT01373281 | Completed | Sanofi Pasteur | |
| Placebo/CYD tetravalent dengue vaccine | NCT01254422 | Completed | Sanofi Pasteur | |
| Placebo/CYD tetravalent dengue vaccine | NCT01134263 | Completed | Sanofi Pasteur | |
| QDenga© | Placebo/TAK-003 tetravalent dengue vaccine | NCT06060067 | Recruiting | Takeda |
| 9vHPV vaccine/TAK-003 tetravalent dengue vaccine | NCT04313244 | Completed | Takeda | |
| Placebo/TAK-003 tetravalent dengue vaccine | NCT03999996 | Completed | Takeda | |
| TAK-003 tetravalent dengue vaccine | NCT03771963 | Completed | Takeda | |
| Placebo/TAK-003 tetravalent dengue vaccine/HAV vaccine | NCT03525119 | Completed | Takeda | |
| Placebo/TAK-003 tetravalent dengue vaccine | NCT03423173 | Completed | Takeda | |
| Placebo/TAK-003 tetravalent dengue vaccine/yellow fever vaccine | NCT03342898 | Completed | Takeda | |
| Placebo/TAK-003 tetravalent dengue vaccine | NCT03341637 | Completed | Takeda | |
| Placebo/TAK-003 tetravalent dengue vaccine | NCT02747927 | Active, not recruiting | Takeda | |
| Dengue Vaccine by Butantan | Placebo/butantan tetravalent dengue vaccine | NCT02406729 | Active, not recruiting | Butantan Institute |
DengVaxia© was the first dengue vaccine to be licensed. It is based on a YFV strain (YF17D) but with the prM and E regions substituted with those from DENV serotypes 1-4[135]. Conducted clinical trials have demonstrated that Deng
QDenga©, on the other hand, is based on a DENV-2 strain, with recombinant strains of the other 3 serotypes[139]. A phase III trial with patients across 8 endemic countries has demonstrated, after 4.5 years, that QDenga© is effective and safe for all 4 DENV serotypes in patients that have been previously infected, but only shows effectiveness against DENV-1 and DENV-2 for dengue naive patients[140]. However, there is no evidence of Qdenga© vaccinees having a higher risk of developing a severe illness, in contrast to what is observed to DengVaxia©. Considering that DengVaxia© is only capable of inducing anti-DENV antibodies against E and prM proteins, that might explain why QDenga© has a higher effectiveness, and also why DengVaxia© vaccinees can develop a higher risk of severity, seen that E and prM proteins are the ones involved in antibody-dependent enhancement.
ZIKV is an enveloped virus that upon infecting humans, primarily through the human-mosquito-human route, con
This virus possesses a single-stranded, positive-sense RNA genome. It encodes proteins associated with the capsid (C), envelope (E), precursor of membrane protein (prM), and non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5). Initially, these proteins are translated into a single polyprotein (5’-C-prM-E-NS1-NS2A-NS2B-NS3-NS4A-NS4B-NS5-3’), which is subsequently cleaved[142,143].
The envelope protein (E) is a surface protein essential for the adsorption and fusion of the viral envelope with the host cell’s plasma membrane[144]. Consequently, it is the primary target for the majority of vaccines in development, as it elicits an innate immune response, triggering the neutralizing antibodies production (nAbs). These vaccines commonly utilize an alignment of the prM and E sequences (prM-E), which has already demonstrated favorable results, generating high levels of nAbs in both immunocompetent and immunocompromised mice[145-147].
The precursor of membrane protein (prM) plays a role in viral maturation and release from cells[148]. Therefore, its inhibition also yields a beneficial response by reducing viral multiplication in tissues. Additionally, the non-structural proteins are involved in the replication of the ZIKV and inhibit the expression of IFN I. As a result, they ensure a less effective immune response[149].
The ZIKV was first isolated in 1947 from a febrile Rhesus monkey in Uganda’s Zika Forest. This was followed by its isolation from Ae. africanus mosquitoes the next year[150]. Human infection was first documented in 1954 in Nigeria[6], with only 14 reported cases over the subsequent fifty years. After this long period, a significant outbreak occurred in 2007 on Yap Island, Micronesia, involving 45 confirmed cases associated with Ae. hensilli mosquitoes, where patients presented with fever, rash, and arthralgia[151] and subsequent outbreaks in French Polynesia revealed severe complications such as Guillain-Barré syndrome and microcephaly resulting from maternal-fetal transmission[147]. The virus rapidly spread across the Pacific[141] and into the Americas, culminating in a major outbreak in Brazil in 2015, with an estimated 440000 to 1.3 million suspected cases[151].
As of May 2024, the WHO reported through its epidemiological update that ninety-two countries in Africa, Oceania, America, Europe, and Asia presented current or previous ZIKV transmission. Sixty other countries across the aforementioned continents have established Ae. aegypti vectors but without known cases of viral transmission[152].
Main vectors of transmission: The vectors of ZIKV transmission, as with all other arboviruses, are arthropods, primarily mosquitoes of the family Culicidae and genus Ae. These mosquitoes inject the virus with their saliva when biting vertebrates such as humans, thereby infecting the host (horizontal transmission)[141,153,154]. These mosquitoes have both sylvatic and urban transmission cycles, with Ae. aegypti being the main cause of outbreaks in urban environments around the world[153]. Furthermore, other species within the family are also responsible for epidemics: Ae. albopictus is associated with the 2007 outbreak in Gabon[4]; Ae. hensilli was identified as the primary cause of the Zika outbreak on the island of Yap in the same year[5,155]. The ZIKV has also been detected in Ae. polynesiensis, Ae. africanus, and even in the common household mosquito Cx. pipiens, among others[150,153,156].
Non-vector means of transmission: The viral transmission is not only limited to horizontal transmission through mos
There are several reports reinforcing the possibility of sexual transmission. It is likely that the viral presence in semen components and tissues associated with the reproductive organs contributes to this infection form[165], since some research has demonstrated that the viral presence in semen components can be substantial even weeks after infection onset[157,166]. The aforementioned reports provide data on confirmed symptomatic infections through positive se
Therefore, considering the possibility of sexual transmission of ZIKV, the use of condoms during sexual intercourse, especially when pregnant, is extremely relevant. This not only helps prevent other sexually transmitted diseases but also reduces the possibility of sexually transmitting ZIKV, thus inhibiting the probability of developing another type of trans
Vertical transmission of pathogens is typically not facilitated, as the placenta acts as a protective barrier for the fetus against invading pathogens, preventing infection from crossing the placental barrier in most cases. The placenta is formed by cellular layers of syncytiotrophoblasts, originating from trophoblasts that merge to form syncytia. These initially penetrate the endometrium to secure the blastocyst and subsequently act as a barrier between maternal and fetal blood. Blastocysts are highly resistant to infections from various viruses and confer viral resistance to non-trophoblast paracrine cells through the release of effectors such as type III IFN[170,171].
However, one of the viruses capable of crossing the placenta is the ZIKV, and its invasion mechanisms remain unclear. The complexity of simulating vertical transmission, all stages of pregnancy, and the fact that the placentas of animals used for analysis usually have significant anatomical differences compared to the human placenta, make it challenging to conduct high-quality research[163,172,173].
Viral tropism, entry, replication and exocytosis: ZIKV has a capsule with surface glycoproteins that facilitate its ad
The viral presence in rodents, humans, and other primates tissue analyses has been detected in placental cells, trophoblasts, endothelium, epithelium, immune cells, mature and progenitor neuronal cells, ocular tissues (cornea, retina, optic nerve, and aqueous humor), and bodily fluids such as tears, saliva, semen, cervical mucus, and urine. There is also infection evidence in the male reproductive system, including testicular cells (Sertoli cells, Leydig cells, and spermatogenic cells), as well as in the female reproductive system in vaginal epithelial cells and uterine fibroblasts[165,178].
Upon entering the cell, the virus begins its replication using the host’s machinery to generate new viral copies. In the ER of the cell, the virus undergoes RNA replication and capsid assembly[179]. The cell then uses reticulophagy to degrade the ER and prevent the maturation of ZIKV. The reticulophagy receptor FAM134B is essential for this process. However, the viral protein NS2B3 cleaves and inactivates FAM134B, preventing reticulophagy and enhancing ZIKV replication[180].
After the virus is assembled in the ER, it is transported to the Golgi complex, undergoing maturation processes and conformational changes, facilitating the subsequent fusion of the mature virus with the plasma membrane and cellular exocytosis[181].
Host intrinsic defenses and IFN inhibition: Upon being infected, a significant portion of the host’s cells have the ca
However, the virus has the ability to inhibit the host’s immune response through various mechanisms. The ZIKV has non-structural proteins responsible for several actions, including the inhibition of IFN production. The NS3 protein can bind to the 14-3-3 protein of RIG-I-like receptors, blocking the translocation of RIG-I and MDA5 to the mitochondria and thereby preventing the pathway for IFN transcription factors from occurring[185]. NS4A acts directly on the mito
Adaptative response and the viral strains: The adaptive response against ZIKV is primarily mediated by CD4+ and CD8+ T cells, playing an important role in inhibiting viral replication, especially when there is inhibition of type I IFN[188]. CD4+ T cells predominantly differentiate into T helper 1 cells during Zika infection, increasing levels of cytokines such as IFN-γ, IL-2, TNF-α, and the transcription factor T-bet, given their crucial role in orchestrating the immune response through cytokine production[189]. CD8+ T cells, in turn, also aid in the release of cytokines like IFN-γ and TNF-α, along with higher expression of granzyme B[189]. B lymphocytes also participate in the adaptive immune response, eventually transforming into plasma cells, ensuring humoral immunity by releasing antibodies against ZIKV. This action is also driven by CD4+ T cells, and one of the main antibodies released are EDIII-specific neutralizing antibodies that neutralize epitopes present in the virus’s EDIII protein[190,191].
The inhibition of CD8+ T cells during infection has been correlated with increased viral infection in the central nervous system (CNS), but with higher survival rates and lower incidence of paralysis[192]. On the other hand, the decrease in CD4+ T cells resulted in paralysis in all studied mice, in addition to increasing the viral load in the CNS and reducing survival[193]. These findings highlight the significant role of CD8+ T cells in neuropathology, as it has been shown that these cells mediate the lysis of virus-infected neurons[189]. Conversely, CD4+ T cells have demonstrated a regulatory function by reducing the immunopathological effects triggered by CD8+ T cells.
Therefore, our immune system, which is responsible for defending the body against pathogens such as ZIKV, has its efficacy dependent on the virus’s ability to evade immune signaling pathways and inhibit IFN production. The different strains of the ZIKV, which emerged after various genetic mutations, also differ in their capacity to manipulate this immune response and are essentially divided into two main lineages with considerably different pathogenic characteristics: The African and Asian lineages.
African strains (such as the East African MR766 and West African lineages) have been shown to induce more potent inflammatory reactions and possess greater virulence[182]. However, the Asian strains (which include contemporary strains from Asia, Oceania, and the Americas) are more strongly associated with neurological disorders and microcephaly present in congenital Zika syndrome[163,194]. The Asian lineage emerged following the viral migration from Africa to Southeast Asia, being detected in Malaysia (1966; P6-740), the Pacific Islands, and later spreading to the Americas[195].
In addition to inhibiting the production and signaling of type I IFN, which is also present in African strains, studies indicate that the Asian strains can prevent the transcription and translocation of INF to the cell nucleus through the actions of NS1, NS4B, and NS5 proteins. This can lead to much more prolonged infections, potentially lasting for months, in contrast to the African strains that typically result in self-limited febrile infections[193,196,197].
Cutaneous pruritus: Pruritus is a frequent symptom in ZIKV -infected patients potentially linked to mast cell degranulation via the IgE-dependent histaminergic itch pathway[164,198]. Mast cells, a type of innate immune system cell, are among the main culprits for the symptomatic manifestation of various inflammatory and allergic reactions, and their G protein-coupled receptors (mainly H1R and H4R) play an important role in the development of cutaneous itching[164,198].
The ZIKV has already shown tropism for the HMC-1 Lineage of mast cells isolated from the human placenta, triggering histamine degranulation and releasing various cytokines, thus being identified as a potential cause of itching during infection[164]. This itching can be alleviated by administering antihistamine medications, thereby reducing this uncomfortable symptom.
Congenital Zika virus syndrome and neuronal tropism: The correlation between Zika infection in pregnant women and microcephaly in their offspring is widely known[199]. However, all the associated mechanisms are not yet completely elucidated. Although, ZIKV effectively replicates in immature neurons in vivo, as shown in studies infecting embryonic mouse brains with the Asian strain SZ01. This replication triggers apoptosis, disrupts the cell cycle, inhibits neural progenitor cell differentiation, and ultimately causes cerebral cortex thinning and microcephaly, a critical factor in the development of human microcephaly[194].
Wu et al[163] also demonstrated vertical transmission in immunocompetent pregnant mice through intraperitoneal injection containing the contemporary Asian strain (ZIKV SZ01) isolated in serum, infecting radial glial cells of the dorsal ventricular zone in offspring with decreased proliferation of cortical neuronal progenitor cells, which are their main target. The infection was shown to affect brain development, reducing the lateral ventricle cavity and cortical surface area. A considerable number increase of IL-17a receptors in brain samples was also observed, likely due to maternal immune activation in response to the virus.
The ZIKV can activate T cells (Th1, Th2, Th9, and Th17), increasing cytokine levels in the acute phase with significant elevation of interleukins IL-1b, IL-2, IL-4, IL-6, IL-9, IL-10, IL-13, and IL-17, decreasing their levels in the subsequent phase (subacute)[178]. However, the action of interleukins can extend beyond their antiviral role, as IL-17a is likely involved in the development of microcephaly in infected humans.
In 2016, a study subjected pregnant rodents to controlled immune response activation by the IL-17a pathway. The results demonstrated impairments in offspring cortical development alongside behavioral abnormalities similar to autism spectrum disorder, with impaired social interactions and considerable phenotypic changes. Blocking IL-17a activity through specific antibodies protected the offspring against brain damage, demonstrating the significant role of this cytokine in the observed alterations, such as fetal brain malformation. Therefore, in addition to the virus’s direct action on CNS cells, cytokine reactions released due to maternal immune activation may also influence the brain damage caused by congenital Zika virus syndrome[200].
Guillain-Barré Syndrome and molecular mimicry: Adults can also develop neurological complications due to the virus’s strong tropism for nervous tissues[165]. One of the most common complications of the infection is Guillain-Barré Syndrome (GBS), an immune-mediated polyradiculoneuropathy that results in axonal neuropathy and is the leading cause of flaccid paralysis worldwide[201].
Data from seven countries in Central and South America showed a significant 2.0 to 9.8-fold increase in GBS cases during ZIKV outbreaks, with subsequent decreases observed once outbreaks were controlled[202]. The presence of antiglycolipid antibodies, mainly against GA1, has been reported by Cao-Lormeau et al[203] in one-third of the analyzed patients diagnosed with GBS having anti-ZIKV IgG or IgM. Other analyses have demonstrated IgM and IgG antiganglioside antibodies in patients under similar conditions[204,205]. This immune response is likely triggered by molecular mimicry between viral structures and neuronal proteins, a situation where the patient’s body begins to recognize parts of its own body as structures of the invading pathogen, causing self-damage.
Among the probable structures involved in molecular mimicry, the neuronal proteins associated with GBS (Heat Shock 70 kDa protein 12A and voltage-dependent L type Calcium channel subunit α-1C) and the glycan loop region of the viral envelope protein E may be responsible for the immune recognition error due to the conservation of an IVNDT motif present in both proteins[206]. This situation ultimately triggers the production of antibodies and an immune response against the myelin sheath of peripheral nerves, thus causing the axonal neuropathy associated with GBS.
Clinical manifestations and major complications: After being transmitted through arthropod bites, the ZIKV enters a period of incubation, which typically lasts between 3- and 12-day following transmission. Notably, only a minority of those infected (20% to 25%) develop symptoms after the incubation period[153,207].
Symptoms are generally mild, nonspecific, and often self-limiting[199], making them easily confusable with other infections, especially those caused by other arboviruses[153]. Therefore, diagnosis should not rely solely on symptoms but also on epidemiological factors, taking into account current endemic and epidemic conditions in the patient’s residence and places they may have traveled.
Concurrent infections are not uncommon[208], especially in regions where common arbovirus vectors are endemic, such as parts of Africa, Asia, and Latin America[152]. Consequently, many symptoms may be erroneously attributed to another pathogen causing simultaneous infection in the host. Laboratory tests are essential allies in diagnosis, particularly for concurrent infections, allowing for the prediction and potential prevention of various complications associated with the involved pathogens, including gestational complications related to ZIKV[209].
Among the signs and symptoms, ZIKV infection can present with a maculopapular rash typically associated with pruritus. This rash usually has a centrifugal distribution, developing in proximal regions and later affecting distal limbs, lasting between one to four days. Fever tends to be mild (between 37.4-38.0 degrees Celsius), unlike the higher fevers associated with the DENV infection[153,199].
Other symptoms such as arthralgia, extremity edema, myalgia, fatigue, mild headache, dizziness, loss of appetite, digestive disturbances, auditory issues, and hypotension may also occur, rarely persisting for more than two weeks[153,199,207]. Retro-orbital pain, commonly linked with dengue, can also arise in ZIKV infections, and conjunctivitis or conjunctival hyperemia is more frequent in ZIKV infections compared to other arboviral infections[153]. Elevated intraocular pressure can also be a complication, potentially leading to glaucoma[210].
Genitourinary symptoms, including hematospermia, have been reported[167]. The virus’s tropism for tissues in this region, as well as its presence in urine, semen, and secretions, is well-documented[157,165,166,199].
One of the most concerning complications of ZIKV infection is microcephaly. Reports from the 2013 outbreak in French Polynesia[211] to the 2015 outbreak in Brazil[212] have highlighted the detrimental impact of ZIKV on ongoing pregnancies. An increase from 20 cases of microcephaly per 10000 live births during the ZIKV outbreak in Brazil, compared to 0.5 per 10000 live births before the outbreak[213], underscores the virus’s aggressive potential in disrupting fetal CNS development.
The virus’s strong neurotropism also poses risks for adults, often underestimated. Besides potentially causing autoimmune complications such as Guillain-Barré Syndrome due to molecular mimicry[201,204,206,214], ZIKV infection has been associated with complications like transverse myelitis, encephalitis, chronic inflammatory demyelinating polyneuropathy, meningitis, seizures, optic neuropathy, and acute demyelinating polyneuropathy[215]. A case-control neuroimaging study demonstrated changes in gray matter volume in certain brain regions post-infection, thereby altering the functional organization and structure of the adult brain[216].
Deaths related to ZIKV infection are rare and typically linked to microcephaly[162]. In 2015, three deaths were reported in Brazil: An adult man with lupus erythematosus, rheumatoid arthritis, chronic corticosteroid use, and a history of alcoholism, a 16-year-old girl, and a newborn[217]. In Colombia, a 15-year-old girl with sickle cell anemia also died following ZIKV infection[218], indicating that comorbidities can increase mortality risk. When ZIKV infection is suspected, the WHO emphasizes the importance of asking the patient about the onset of symptoms. This information guides the selection of appropriate laboratory tests based on the duration of symptoms. A thorough travel history, especially if travel occurred within the past two weeks, should be obtained, including dates, locations, and duration of travel, as well as possible sexual contact with confirmed Zika cases, breastfeeding status, and recent vaccinations, particularly against other flaviviruses such as YFV, Japanese Encephalitis, and dengue[219].
Laboratory diagnosis: The laboratory diagnosis of ZIKV is typically performed using ELISAs to detect the presence of anti-ZIKV IgM and IgG antibodies. IgM is detectable from 5 days to 12 weeks after the onset of symptoms, whereas IgG antibodies appear a few days after IgM detection and usually remain detectable for over a year[220-222].
ELISA is generally a less complex, quicker, and cheaper method compared to other tests still used worldwide, such as the PRNT, fluorescent antibody test, hemagglutination-inhibition test, and complement fixation test[223]. However, false-positive and false-negative (particularly in immunocompromised patients with inadequate adaptive immune responses or when tests are conducted before the onset of the antibody-associated adaptive immune response) results for IgM and IgG tests are still significantly reported. Cross-reactivity, especially with viruses from the same family (Flaviviridae)[221], remains a common issue in these tests, potentially leading to incorrect diagnoses.
Therefore, PRNT can be used to confirm laboratory diagnoses by quantifying neutralizing antibodies in serum or cerebrospinal fluid (CSF) samples more specifically, serving as the gold standard for diagnosis[223]. For viral RNA detection, RT-PCR can be utilized during the infection, offering high sensitivity and specificity[141,155,223,224].
However, these tests are not very compatible with common outpatient settings, as they require appropriate in
According to the WHO[219], laboratory diagnosis can be conducted using serum, whole blood, or urine samples. Other samples may be considered when neurological complications related to ZIKV infection are suspected, including in cases of a sexual transmission suspected, as semen samples, since the virus tends to persist longer in urine and semen tests compared to blood analyses[166,227].
For patients within 7 days of symptom onset, nucleic acid tests (NAT), such as RT-PCR, are recommended to diagnose viral presence. For those with more than 7 days of symptoms, serological detection tests for IgM antibodies (ELISA), present in the acute phase of infection, can be used. NAT can also be employed, although negative results do not rule out infection since viremia may be low after one week of symptom onset[219]. IgG detection just indicates a past infection that elicited an immune memory response.
During outbreak periods, the WHO recommends prioritizing testing for a select group of patients[219] as there is normally a limited number of tests available to be used (Table 2).
| No. | Priority recommendation for viral testing during periods of ZIKV outbreak-WHO |
| 1 | Symptomatic patients who have had sexual relations with a partner with probable or confirmed infection |
| 2 | Suspected patients with neurological complications |
| 3 | Pregnant women with a travel history to endemic areas, residents in endemic areas or those in current outbreak regions |
| 4 | Pregnant women who have had sexual relations with a confirmed or probably infected patient |
| 5 | Pregnant women with suspected or confirmed fetal brain anomalies who have a travel history to endemic areas or reside in endemic areas or current outbreak regions |
| 6 | Women who have had miscarriages or stillbirths and traveled or resided in Zika virus-affected areas during pregnancy |
| 7 | Infants born with microcephaly or neurological complications whose mothers traveled or resided in endemic areas or current outbreak regions |
| 8 | Breastfeeding infants with mothers diagnosed with the viral infection |
Findings in complementary exams: During ZIKV infection, additional exams are commonly requested to assist in the clinical management of the patient. However, reports contain limited information about other laboratory exams performed. The results of a complete blood count and leukogram are usually normal, without leukopenia or thrombocytopenia, which are common in CHIKV and DENV infections[153]. The patient may show slight elevations in C-reactive protein, ferritin, and fibrinogen, as well as increased serum lactate dehydrogenase and liver enzymes, findings commonly seen in other viral infections[153,199]. These clinical data have little impact on the management of ZIKV infection, as the disease lacks research indicating a likelihood of a worse outcome even when the patient presents such altered exams.
Treatment: There is no specific treatment for ZIKV. However, appropriate management focuses on alleviating symptoms. The WHO recommends using antipyretics for patients with fever, antihistamines for those with itching, and analgesics for pain relief. Adequate hydration and rest can also aid in the patient’s recovery[228].
The use of NSAIDs is contraindicated without completely ruling out DENV infection, as there is a risk of hemorrhagic complications[228]. Additionally, NSAIDs are contraindicated in pregnant women after the 32nd week of gestation regardless of the infecting virus, due to the risk of premature closure of the ductus arteriosus[229]. Administration of acetylsalicylic acid is also contraindicated, as it increases the risk of developing Reye’s syndrome[229].
However, even if the current treatment is still just medication to alleviate the symptoms of the infection, various compounds have been studied in recent years as anti-flavivirus substances and may be available on the market for infection treatment in the coming years. An ideal drug should possess the ability to penetrate the blood-brain barrier, characterized by small and/or lipophilic molecules. Additionally, it should target the infection’s host cells, such as fetal neural progenitor cells, exhibit placental penetrance to prevent vertical transmission, and be highly safe for administration to pregnant women[230].
The coinfection and cocirculation of flaviviruses like DENV, YFV, Mayaro, and Oropouche virus in various parts of the world infect hosts and cause immune responses with cross-reactivity. This has led researchers to conclude that the best option for developing an anti-ZIKV drug would also be one that protects against other flaviviruses. This is because the structures of several studied target proteins are similar, and recently developed preclinical compounds have shown activity against multiple flaviviruses, making them promising candidates for medication[230].
Consequently, considering the most promising proteins for the development of this medicine when examining host factors associated with infection, the TIM1 binding protein proves to be a significant factor for the binding of the viral phospholipid during ZIKV entry. However, it is also involved in the infection of DENV-2 and West Nile virus, making it an interesting target for a multi-flavivirus drug[230,231]. Inhibitors of the E protein binding to host receptors also show potential as drug targets, thus preventing viral adsorption. Nevertheless, one of the most promising targets for drug creation is certainly viral RNA-dependent RNA polymerases (RdRp), as they are extensively studied targets with substantial literature supporting their efficacy and safety[232]. By inhibiting RdRp, viral replication and the production of infectious particles are also inhibited.
To understand the importance of RdRp in the virus replication cycle, research shows that Zika, being part of a genus of single-stranded positive-sense RNA viruses, has RdRp proteins that synthesize a complementary (negative-sense) strand used to synthesize new positive-sense strands, which will later be used as mRNA in virus replication. In ZIKV, the RdRp protein responsible for creating new strands is NS5, which also suppresses type I IFN and is the focus of various drugs currently being developed.
The RdRp inhibitors have been successful in treating other viruses such as hepatitis C virus, HIV, and herpes simplex virus. A ProTide technology nucleoside analog for HCV, already approved by the FDA (Sofosbuvir), has shown significant effects and high safety as an anti-ZIKV agent both in vivo in mice (demonstrating prevention of vertical transmission and reduced morbidity) and in vitro in neuronal cells. Sofosbuvir is classified as category B for administration in pregnant women, meaning that while there are no controlled studies in pregnant women, animal studies have not shown risk to the fetus.
Conversely, analogs of Sofosbuvir (such as 2’-C-ethynyluridine aryoxyl phosphoramidate and 2’-C-methyluridine aryoxyl phosphoramidate) have demonstrated superior anti-ZIKV effects compared to the medication. However, clinical trials are also necessary to prove their safety in pregnant women and efficacy against sexual and vertical transmission.
Finally, other potential preclinical compounds under investigation include protease inhibitors, viral assembly inhibitors, inhibitors of ZIKV fusion to the cell membrane, nucleoside biosynthesis inhibitors, and ZIKV antivirals targeting the host. These drugs are still being evaluated for safety and efficacy.
Prevention: Preventive measures range from personal care, such as using effective repellents containing DEET, IR3535, or icaridin, and wearing long clothing that covers as much skin as possible, especially in areas known to have ZIKV vectors, to collective measures, like eliminating potential breeding sites where water can accumulate. Special caution is advised during the peak activity times of the major urban vector, Ae. aegypti (early morning and late afternoon), using mosquito nets, window and door screens, and electric repellents at home to aid in prevention[228].
During pregnancy, women are advised not to travel to endemic or outbreak areas. Ultrasound scans to monitor fetal development are recommended every 3 to 4 weeks for patients with confirmed or suspected ZIKV infection, and newborns should be tested at birth[209].
Furthermore, regarding men, the WHO also advises that those who have traveled to endemic or outbreak areas should avoid sexual relations with their pregnant partners or use condoms for up to three months after exposure[228].
Vaccines in development: Successful flavivirus vaccines, such as the current dengue vaccine (Qdenga) from Takeda, along with knowledge of ZIKV pathogenesis and general characteristics, are key factors directly influencing the advancements in the development of various ZIKV vaccines. Nucleic acid vaccines (DNA and mRNA), inactivated virus vaccines, live attenuated virus vaccines, viral-vectored vaccines, virus-like particle (VLP) vaccines, protein antigen-based vaccines, and mosquito saliva antigen-based vaccines are all in preclinical or clinical stages of human testing[145,146].
Currently, more than 50 ZIKV vaccines are under development and a large portion is detailed on the ClinicalTrials.gov website, a global database maintained by the National Library of Medicine[233]. However, the WHO and the National Institutes of Health (NIH) report that Phase III field efficacy trials become unfeasible in the absence of a new outbreak, thus hindering effective human trials and subsequent approvals[234](Table 3). Finally, the lack of substantial investment from both private and governmental initiatives also delays the development process.
| Vaccine technology platforms | Intervention/treatment | ClinicalTrials.gov ID | Phase | Status | Sponsor |
| DNA vaccine | Biological: VRC-ZKADNA090-00-VP; Other: VRC-PBSPLA043-00-VP | NCT03110770 | 2 | Completed | NIAID |
| Biological: VRC-ZKADNA090-00-VP | NCT02996461 | 1 | Completed | NIAID | |
| Biological: VRC-ZKADNA085-00-VP | NCT02840487 | 1 | Completed | NIAID | |
| mRNA vaccine | Placebo/biological: mRNA-1325 | NCT03014089 | 1 | Completed | ModernaTX, Inc. |
| Placebo/biological: mRNA-1893 | NCT04064905 | 1 | Completed | ModernaTX, Inc. | |
| Placebo/biological: mRNA-1893 | NCT04917861 | 2 | Active, Not Recruiting | ModernaTX, Inc. | |
| Viral vectored vaccine | Placebo/biological: MV-ZIKA-RSP vaccinations (high or low doses) | NCT04033068 | 1 | Completed | Themis Bioscience GmbH |
| Biological: ChAdOx1 Zika | NCT04015648 | 1 | Completed | University of Oxford | |
| Placebo/biological: MV-ZIKA | NCT02996890 | 1 | Completed | Themis Bioscience GmbH | |
| Live attenuated vaccine | Placebo/biological: rZIKV/D4Δ30-713 | NCT03611946 | 1 | Completed | NIAID |
| Purified inactivated vaccine | Placebo/biological: VLA1601 | NCT03425149 | 1 | Completed | Valneva Austria GmbH |
| Placebo/biological: Zika virus purified inactivated vaccine | NCT02937233 | 1 | Completed | Kathryn Stephenson | |
| Biological: VLA1601/CpG 1018®/3M-052-AF | NCT06334393 | 1 | Recruiting | Valneva Austria GmbH | |
| Placebo/biological: PIZV | NCT03343626 | 1 | Completed | Takeda | |
| Placebo/biological: Zika virus purified inactivated vaccine | NCT03008122 | 1 | Completed | NIAID | |
| Placebo/biological: IXIARO; YF Vax 17D strain and Zika virus purified inactivated vaccine | NCT02963909 | 1 | Completed | NIAID | |
| Drug: Saline/biological: Zika virus purified inactivated vaccine | NCT02952833 | 1 | Completed | NIAID |
According to the WHO and the United Nations International Children’s Emergency Fund (UNICEF), the target product against ZIKV should provide adequate protection against congenital Zika syndrome, particularly focusing on the immunization of women of childbearing age and pregnant women[235]. Innovative technologies recently developed, such as mRNA vaccines authorized to treat COVID-19[236], can be a promising alternative for ZIKV immunization, especially after the successful performance observed during the pandemic[237,238].
Inactivated virus vaccines are generally safe, even for pregnant women and immunocompromised individuals, making them an ideal candidate for preventing congenital Zika syndrome. However, this type of vaccine typically requires higher doses to ensure an adequate and long-lasting immune response. On the other hand, live attenuated virus vaccines usually elicit efficient immune responses from the first dose and tend to provide a much more durable immune response. However, given the pathogenesis of ZIKV, this type of vaccine may not be ideal for pregnant women due to the potential for maternal-fetal transmission and associated complications[239].
Probably, the combination of various types of vaccines that may become available on the market in the coming years will offer greater benefits to the population, as they have diverse indications, contraindications, and benefits.
Yellow fever (YF) is caused by the YFV and has historically been one of the world’s most lethal and feared diseases. YFV belongs to the Flaviviridae family and is one of over 70 members of the Flavivirus genus, with “flavus” being the Latin word for yellow. The virion has a spherical shape with a diameter of 40-50 nm[143]. Its genome consists of a single-stranded positive-sense RNA of approximately 10.8 kb, containing an open reading frame that encodes a single polyprotein of 3411 amino acids[240], which is post-translationally cleaved to produce mature viral proteins. These viral proteins are classified as structural and non-structural. Despite having different genotypes, the YFV has a single serotype[241].
The structural proteins crucial for the formation and structure of the virion include the capsid protein C, the pre-membrane protein prM, and the envelope protein E, which together constitute the viral particle[242]. The transmembrane domains of the prM and E proteins act as localization signals to the ER, containing specific sequences that direct these proteins to the ER[243]. Notably, the E protein plays a crucial role in recognizing and binding to host cell receptors, facilitating viral entry[244], and is an important target of the immune system during YFV infection, triggering the pro
YF is a zoonotic viral disease endemic to various tropical regions in Africa and the Americas, characterized by a transmission dynamic involving non-human primates (NHP) reservoir and humans, mediated by mosquito vectors. The YFV is primarily transmitted to humans by primates through the bite of infected mosquitoes, posteriorly establishing a human-mosquito-human transmission cycle[247]. This interaction can result in a wide range of symptoms, from mild fever to severe liver disease and jaundice, the latter giving the disease its name[241]. Effective transmission control and a thorough understanding of the virus-host interaction are crucial for the management of the disease.
Although YF cannot be eradicated, epidemics can be prevented through mass immunization of the population and the maintenance of routine childhood vaccinations. Low vaccination coverage has led to significant outbreaks in Angola (2015-2016), the Democratic Republic of Congo (2016), and Brazil (2017-2018)[248], highlighting the urgent need to address this gap. Consequently, in 2016, to combat and eliminate the growing urban outbreaks of YFV and prevent its international spread, the WHO, in partnership with UNICEF and Gavi, launched the Eliminate Yellow Fever Epidemics initiative. This initiative has strategic objectives to protect at-risk populations, prevent the international spread of YFV, and quickly contain outbreaks. One of its key actions is mass vaccination campaigns, with an estimate to have over one billion people properly vaccinated by 2026[249].
Phylogenetic analyses suggest that the virus, which gave rise to the currently circulating strains, originated in Africa within the last 1500 years and was introduced to the Americas around 300-400 years ago during the transatlantic slave trade[250]. The first recorded epidemic occurred in Yucatan in 1648[251]. The Spanish-American War highlighted the disease’s impact, with more soldiers dying from YF than combat in Cuba invasions. Walter Reed’s research between 1899 and 1901 confirmed mosquito transmission of the virus[251,252]. The isolation of the virus from a patient named Asibi in 1927 led to the development of the 17D vaccine by Max Theiler, who received a Nobel Prize for this achievement in 1936[253].
As of 2023, the WHO reports that YF remains endemic in 34 African countries and 13 countries in Central and South America[254]. Ongoing vaccination efforts and surveillance are vital to prevent outbreaks and control the spread of the disease. The 17D vaccine continues to be a cornerstone in the fight against YF, highlighting the importance of immunization programs in endemic regions.
Transmission cycle: YF is a zoonotic infection transmitted from primates to humans through the bite of infected mosquitoes[241]. The virus is inoculated into the host via the mosquito’s saliva. After an incubation period of 3 to 7 days, viremic hosts can infect other mosquitoes that feed on their blood, thus continuing the transmission cycle. Mosquitoes remain infected for life and can pass the virus to their eggs through transovarial transmission[255,256].
YFV has different transmission cycles: Sylvatic, urban, and intermediate. In the sylvatic cycle, transmission occurs in forested areas between blood-feeding mosquitoes and NHP. In the Americas, the primary vectors are mosquitoes of the Haemagogus and Sabethes genera, while in Africa, Aedes mosquitoes predominate. NHPs are the natural hosts of the virus. Following urbanization, YF entered the urban cycle, where transmission occurs among humans in urban and peri-urban areas, with Ae. aegypti being the primary vector[257]. There is a high risk of outbreaks when infected humans from forest areas travel to densely populated areas with low immunity to the virus, where vector mosquitoes are present[258].
In addition to the sylvatic cycle, there is an intermediate transmission cycle for YF. Small epidemics can occur at the edges of African savanna forests, in humid and semi-humid zones, known as emergent zones, where humans come into contact with the wild cycle. In this cycle, transmission occurs among NHPs, humans, and mosquitoes, such as Ae. africanus[257].
The recent detection of Ae. albopictus mosquitoes contaminated with YFV in urban and rural areas around the world is concerning and needs attention[259]. Additionally, transmission can occur through other routes, such as exposure to infected blood and aerosols in laboratories[260]. Cases of perinatal transmission to newborns have also been reported[261,262]. Furthermore, the attenuated 17D vaccine strain of the virus has been reported to be transmissible through blood transfusion[263], organ transplantation[264] and, in rare cases, breastfeeding[265,266]. An investigation in the United States in 2021 revealed that transmission of the YF vaccine virus virus via organ transplantation and blood transfusion caused severe neurological disease and fatalities in four recipients. These findings suggest that after receiving a vaccine dose, blood donation should be delayed for at least two weeks[264]. Continuous surveillance and adequate vaccination are essential to prevent outbreaks.
Binding and entry: After the inoculation of the virus, the process of viral replication and dissemination to other tissues begins. In the Flaviviridae family, viral replication occurs through the synthesis of an antigenome template used for the production of genomic RNA and the synthesis of viral proteins[267]. The entry of flaviviruses into their target cells is mediated by the interaction of the E glycoprotein with receptor molecules on the cell surface, promoting fusion with the cell membrane for viral entry[268]. However, the host cell receptors that bind to the E glycoprotein have not yet been identified[269]. The DIII domain of the E protein is considered the receptor-binding domain of flaviviruses[244,270-273].
YFV binds non-specifically to heparan sulfate on the surface of host cells, such as hepatocytes and dendritic cells[274,275]. Despite using different pathways, both wild-type and attenuated strains of YFV employ a pH-dependent entry mechanism[276]. The wild-type Asibi strain enters host cells through clathrin-mediated endocytosis, while the attenuated YFV-17D strain utilizes a clathrin-independent pathway[277]. The conformational rearrangement of the E glycoprotein occurs in the lower pH environment of the endosome, facilitating the fusion of the viral lipid envelope with the endosomal membrane[278].
It is important to note that the valosin-containing protein (VCP/p97), a cellular ATPase that unfolds and extracts ubiquitinated client proteins from large complexes, has been reported as a factor with various functions in flavivirus replication, such as viral uncoating[279]. Consequently, the viral genome is released into the host cell cytoplasm.
After the flavivirus RNA enters the host cell, the viral genome acts as messenger RNA (mRNA) and is translated at the rough ER into a polyprotein, anchored in the ER itself[280]. This polyprotein is cleaved by cellular peptidases and viral proteases NS2B/3[281-283].
The NS5 protein is particularly notable as it houses the methyltransferase and RdRp domains, which play a crucial role in viral RNA synthesis and regulation of replication processes[284], providing insights into targets for the development of therapeutic strategies[241]. Additionally, it is suggested that G protein-coupled receptor kinase 2 contributes to various stages of the virus life cycle by enhancing both viral entry and RNA synthesis, being a regulator of flavivirus infection[285].
Host factors play essential roles in this process: The signal peptidase complex associated with the ER (SPCS) is responsible for processing the Pr-E junction and secreting viral particles[286]; the DNAJC14 protein, a Hsp40 cocha
Following this processing, the viral RNA replication complex is assembled by non-structural proteins such as NS1, NS2B, NS3, NS4A, NS4B, and NS5. The NS4A protein induces rearrangements in the ER membrane, promoting active viral RNA replication, which is then packaged forming the virion[290]. These immature virions are secreted in vesicles and transported to the Golgi apparatus, where they traverse chambers with increasingly lower pH. The enzyme furin cleaves the viral envelope proteins, resulting in mature virions that are then released by exocytosis[291,292].
Immune response: The understanding of the pathogenic mechanisms of the YFV remains limited, primarily due to the lack of animal models that accurately reproduce the disease observed in humans[269]. Current knowledge is largely based on human tissue biopsies from fatal YF cases and indirect observations made in animal models[293], which do not fully capture the characteristics of human infection.
Upon being bitten, the infected mosquito injects the YFV into the skin. The virus is then recognized by APCs, such as dendritic cells, which activate PRRs, including RIG-I-like receptor (RLR) family[294] and TLRs such as TLR-2, 7, 8, and 9. This activation leads to the production of pro-inflammatory mediators and type I IFNs (such as IFN-α and IFN-β). These IFNs play a fundamental role in the antiviral response by promoting an antiviral state in adjacent cells and activating immune cells, which trigger multifaceted immune responses to present the antigen to CD4+ T lymphocytes in lymphoid tissues like the spleen and lymph nodes[295]. Plasmacytoid dendritic cells (pDCs) produce IFNs in response to YFV in a TLR-7-dependent manner, with this stimulation being more effective with immature viral particles[296]. In addition to this, antiviral response is mediated by RNA-sensing proteins like RIG-I and protein kinase R, which induce pro-inflammatory cytokines upon detection of viral genetic material independently of stress granules[297].
Studies have demonstrated that the viral non-structural protein NS5 interacts with the human transcription factor hSTAT2, induced by IFN-1, playing a crucial role in modulating the host’s immune response, viral replication, and determining the tropism of YFV. This interaction allows the virus to evade type I IFN-mediated antiviral defenses[298,299]. YFV uses its NS5 protein to inhibit IFN-I signaling by interacting with STAT2, a process dependent on IFN-I-induced modifications, specifically STAT1 phosphorylation and NS5 polyubiquitination by TRIM23[300,301].
APCs like macrophages and dendritic cells are crucial in activating Th1-type CD4+ T lymphocytes, where antigens are presented on the surface of APCs via class II major histocompatibility complex molecules, recognized by T cell receptors[302]. The immune response against YFV begins with innate immunity, the body’s first line of defense. Dendritic cells (S100+), present in tissues such as the skin and liver, are among the first to detect YFV. They phagocytize the virus and present its antigens to the adaptive immune system. Macrophages (CD68+), in addition to phagocytizing the virus and infected cells, secrete cytokines and inflammatory mediators, including reactive oxygen species, nitric oxide (NO), and TNF-α, which promote inflammation and recruit other immune cells to the infection site[303]. This release of inflammatory substances and cytokines, causes a “cytokine storm” that triggers disturbances. Consequently, there is midzonal apoptosis of hepatocytes, along with pathological changes like heart apoptosis and acute tubular necrosis in renal tissues[302]. Regarding serum markers, elevated levels of IL-6, MCP-1, IP-10, TNF-α, and IL-1RA were found in the sera of YFV-infected patients who had fatal outcomes compared to those with non-fatal outcomes[304].
Adaptive immunity is triggered when dendritic cells present viral antigens to CD4+ T cells. These helper T cells proliferate and release cytokines that activate other immune cells. In fatal YF cases, CD4+ T cells are predominant and crucial for coordinating the immune response[303]. CD8+ T lymphocytes target and lyse virus-infected liver cells, releasing viral particles that expose antigens to B lymphocyte-produced antibodies. B lymphocytes (CD20+), activated by helper T cells, produce specific antibodies that neutralize YFV, prevent viral entry into new cells, and mark the virus for destruction by macrophages[305].
Hepatic damage: The liver is particularly affected in YF. Immunohistochemical studies on the livers of patients who succumbed to the disease have revealed damage characterized by macro/microvesicular steatosis, apoptosis, and necrosis, especially in the intermediate zone of the liver, where viral antigens were most frequently observed[306].
Studies in animal models[293,307-310] and human tissue biopsies from fatal cases[303,306,311,312] highlight apoptosis as a central mechanism in the pathogenesis of YF, attributed not only to the cytopathic effect (CPE) induced by the virus but also to an imbalanced cytokine response.
The inflammatory infiltrate in the liver of fatal YF cases predominantly consists of CD4+ T lymphocytes, with smaller quantities of CD8+ T lymphocytes, macrophages CD68+, CD20+ B lymphocytes, NKT+ cells, and S100+ dendritic cells[303,311]. Cytokine expression is also notable, with significant numbers of cells expressing TGF-β, and to a lesser extent, TNF-α and IFN-γ[311]. Apoptosis, rather than necrosis, has been identified as the primary mechanism of cell death during infection, likely influenced by viral antigens and the presence of TGF-β, an apoptosis-inducing cytokine responsible for the downregulation of inflammatory infiltrates observed in the liver of fatal cases[303,306,311]. The interaction between the Fas receptor (CD95) and its ligand FasL, induced by TGF-β, is one of the mechanisms by which CD8+ T cells promote the apoptosis of infected cells, thereby limiting viral spread[312]. Other apoptotic markers are also found in the hepatic parenchyma, including CASPASE 3, CASPASE 8, BAX, GRANZYME B, and SURVIVIN[313]. These mechanisms contribute to the pathology observed in fatal cases and various symptoms associated such vascular leak syndrome, thrombocytopenia, changes in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, elevated blood urea nitrogen and creatinine, jaundice, vomiting, and hemorrhagic diathesis[302,311].
In situ studies suggest that viral infection activates the endothelium, exacerbating the inflammatory response in the liver. This occurs through the increased expression of adhesion molecules such as E-selectin, P-selectin, ICAM-1, VCAM-1, and VLA-4, which facilitate the adhesion and migration of inflammatory cells into the hepatic parenchyma, con
Moreover, histopathological and immunohistochemical analyses of fatal YF patients revealed a predominant ex
Research indicates that inositol trisphosphate receptor type 3 (ITPR3), a calcium channel isoform, expressed in hepatocytes infected by the virus, can stimulate hepatocyte proliferation and reduce both steatosis and cell death, thereby protecting the organ against insufficiency. This protective mechanism implies that enhancing ITPR3 expression could be an effective therapeutic intervention to prevent the progression of liver failure and reduce mortality, potentially eli
Clinical manifestation: The YFV is predominantly viscerotropic, primarily affecting the liver, as well as organs such as the kidneys, spleen, lymph nodes, and heart[241]. The disease classically manifests in three stages: Infection, remission, and intoxication. These stages are often not well demarcated[320].
In the first stage, the acute infection phase occurs approximately 3 to 6 days after the mosquito bite, presenting clinical characteristics such as high fever (approximately 39 °C), headache, malaise, photophobia, back pain, myalgia, irritability, restlessness, nausea, and vomiting, as well as conjunctival infection, white tongue with a red tip, and bradycardia (Faget’s sign)[302,321]. During this phase, viremia occurs, where the virus replicates and disseminates through the bloodstream, making the host infectious to vectors. Laboratory findings may demonstrate leukopenia, neutropenia, and low C-reactive protein; elevated transaminases and proteinuria may also occur. Only about 45% of infected individuals exhibit symptoms[322].
Next, the remission stage begins, characterized by a temporary improvement in symptoms, lasting between 12 hours and 2 days. The final stage is the intoxication stage, marked by an exacerbated inflammatory response associated with hemodynamic collapse, where there is a sudden deterioration of the patient’s clinical condition, with typical signs of liver and kidney failure, hemorrhagic fever, and multiple organ dysfunction. Liver dysfunction results from apoptosis with limited inflammation and manifests with elevated transaminases and bilirubin, as well as decreased synthesis of coagulation factors produced by the liver[241,303]. Patients may present with jaundice, oliguria or anuria, cardiovascular instability, and hemorrhagic diathesis[302,321]. Notably, about 12% of infected individuals reach this phase, of which approximately 47% succumb to the disease[322].
In the intoxication stage of YF, various laboratory and pathophysiological changes occur that reflect the severity of the disease, including thrombocytopenia with platelet counts below 50000 per milliliter; prolonged coagulation time and prothrombin time; decreased hepatic coagulation factors; decreased fibrinogen and factor VIII; and elevated fibrin degradation products, characteristic of disseminated intravascular coagulation[323,324].
The increase in AST/SGOT can exceed that of ALT/SGPT, which differs from other forms of viral hepatitis and may be related to skeletal or cardiac muscle injuries[241,325].
Laboratory diagnosis: Due to the numerous differential diagnoses stemming from the similarity of symptoms with a wide range of diseases, such as dengue, leptospirosis, viral hepatitis, malaria, and other hemorrhagic diseases, the clinical diagnosis of YF is challenging. Therefore, laboratory confirmation plays an essential role[320]. Laboratory diagnostic methods for YF are crucial to accurately identify the infection in suspected cases. According to the WHO, a suspected case is defined as any person with an acute onset of fever, accompanied by jaundice within 14 days of the onset of initial symptoms[326]. However, this categorization remains restrictive as the disease progresses to jaundice only in its more advanced stages (Table 4).
| Classification | Criteria |
| Probable case | A suspected case and at least one of the following |
| Presence of YF IgM antibody in the absence of YF immunization within 30 days of illness onset | |
| Epidemiological link to a confirmed case or an outbreak (e.g., household members or persons in close proximity through work, residence in past month) | |
| Confirmed case | A probable case and at least one of the following |
| Negative results of differential neutralization testing with flaviviruses endemic in the area of exposure | |
| Seroconversion in appropriately paired samples tested by YF neutralization testing | |
| And absence of YF immunization within 30 days before onset of illness | |
| Or a suspected case and at least one of the following | |
| Detection of YFV genome in blood or other organs by real-time reverse transcriptase polymerase chain reaction | |
| Detection of YF antigen in liver or other organs by immunohistochemistry | |
| Isolation of YF virus | |
| And absence of YF immunization within 14 days before onset of illness | |
| Discarded case | A person who tests negative for YF antibody testing (with specimen collected > 7 days post onset) |
| Or negative immunohistochemistry on tissue samples |
Laboratory tests for YF diagnosis, performed on blood, serum, CSF, urine, or other tissue samples, can be conducted through serological methods, viral isolation, viral genome detection, and viral antigen detection[259].
The most commonly used serological procedure is the detection of anti-YFV antibodies by IgM-ELISA, which offers a presumptive diagnosis of YF within a few hours[241]. The accuracy of this test for detecting YF is generally regarded as high, with a minimum precision of 90%[259]. However, case confirmation requires evaluation of the epidemiological context, detailed vaccination history of the individual, timing of sample collection, and potential co-circulation of other flaviviruses in the region[259]. It is important to consider that this type of test may present limitations, including cross-reactions with other flaviviruses and the need for additional confirmation[327].
NS1 antigen capture ELISA assays have proven efficient for early diagnosis of YF, with high sensitivity and no cross-reactions with other flaviviruses[328]. In serological tests, the PRNT, also known as the virus neutralization test, is more specific for the detection of anti-YFV antibodies compared to other assays and is considered the “gold standard” for differential diagnosis of flaviviruses[329]. However, the requirement for specific cell culture facilities, standardized controls, and well-trained personnel for reproducible results, as well as the 4-7 days needed for result analysis, limit the use of this method during outbreaks[320]. Another technique commonly used to identify IgM and IgG antibodies against the YFV is the indirect immunofluorescence[330].
For viral genome detection, the RT-PCR technique is highly sensitive, capable of detecting YFV in the early stages of infection, even before clinical symptoms manifest. Additionally, RT-PCR can distinguish between wild and vaccine strains of YFV, making it useful for monitoring viral spread and evaluating vaccination strategies[331,332]. Furthermore, other molecular approaches, such as loop-mediated isothermal amplification (LAMP)[333] and reverse transcription-mediated amplification (RT-LAMP)[334,335], offer the possibility of rapid and sensitive YFV diagnosis in field settings without requiring complex equipment.
Treatment, care and prophylaxis in the management of infection: YF presents a significant challenge for healthcare professionals, as it is a severe viral hemorrhagic disease requiring early diagnosis despite often having nonspecific symptoms. There is no specific therapeutic treatment for YF, and its management relies on supportive care. The Pan American Health Organization categorizes YF patients into three groups, corresponding to the classic phases of the disease[241] and reflecting its severity: Group A for mild cases, Group B for patients in remission, and Group C for severe forms with hepatic and renal complications[336].
Due to the potential for rapid disease progression, it is crucial to monitor the warning signs and risk factors associated with YF. For confirmed cases in the infection phase (Group A), attention should be paid to alarm signs such as dehydration, vomiting, diarrhea, abdominal pain, and mild bleeding. Clinical findings such as AST levels more than five times the upper limit of normal, platelet count below 50000/mm³, and proteinuria are also significant[336]. These findings are associated with hepatic damage, hemorrhage risk, and renal impairment[337], respectively. Clinical management in this group includes oral and/or intravenous hydration, pain and fever control using dipyrone (maximum 8 g per day) and acetaminophen (maximum 2 g per day), taking into account the patient’s hepatic condition and avoiding the use of NSAIDs. It is noteworthy that these medication recommendations may not be applicable worldwide, as the use of dipyrone is restricted in several countries.
For Groups B and C, the required level of attention increases due to the worsening of the patient’s overall condition. Severe signs and symptoms at this stage include clinical findings such as jaundice, oliguria, mental confusion, seizures, hemorrhagic phenomena, tachypnea, hypotension, and signs of poor blood perfusion. Group B requires hospitalization, as patients in this group experience dehydration, multiple episodes of vomiting, nausea, diarrhea, altered urinary output, and hemodynamic instability, which may progress to shock. Finally, Group C patients exhibit characteristic signs of hepatic failure, acute renal failure, and hepatic encephalopathy, necessitating intensive care unit (ICU) support with advanced care[336].
Antiviral therapies have not yet been formally recommended for the treatment of YF. However, there is evidence supporting the efficacy of such therapies, including the use of sofosbuvir (an NS5 RNA-dependent RNA polymerase inhibitor), an antiviral drug used against hepatitis C, which has demonstrated antiviral activity against YFV in vitro and in vivo[338,339]. An off-label cohort study using sofosbuvir in YF patients suggested that this medication reduces the viral load of the virus in these patients[340].
Currently, there is no predictive model for the severity and mortality caused by the YFV[336]. However, during the YF epidemic in Brazil, several studies evaluated these parameters. A study conducted on patients admitted to a Brazilian ICU during the 2017 and 2018 outbreaks indicated that factors such as PT-INR, APACHE II, and grade IV hepatic encephalopathy were significant prognostic indicators of mortality risk, independent of other factors[341]. Another 2018 study in São Paulo found that advanced age, high neutrophil count, elevated creatinine, increased AST, and higher viral load were independently associated with higher mortality in YF cases[342]. Additionally, another study demonstrated a higher mortality rate for patients with a history of diabetes mellitus compared to those without this condition. This study also showed that prophylactic use of anticonvulsants for patients with hepatic encephalopathy or arterial ammonia levels above 70 μmol/L reduced the frequency of seizures from 28% to 17%[343]. Furthermore, early aggressive hemodialysis, routine use of intravenous proton pump inhibitors, and plasma exchange were found to be beneficial[343].
Vaccines: Currently, all YF vaccines are derived from the 17D vaccine strain. Vaccination is the most important measure for preventing YF, being safe, accessible, and capable of providing lifelong immunity with a single dose. The YFV has seven genotypes, but only one serotype[241], ensuring that a single vaccine can protect individuals against all genotypes.
The immune response to the attenuated 17D virus (YF-17D) is mediated by both innate and adaptive immune mechanisms. The virus induces a strong innate immune response, triggered by the TLR-2, 7, 8, and 9 receptors on dendritic cells, leading to the production of pro-inflammatory mediators and type 1 IFNs[295]. The stimulation of these receptors induces a balanced Th1 and Th2 immune response[344]. Additionally, pDCs activate downstream signaling pathways that contribute to the antiviral state[252]. Notably, the complement system also plays a role in the innate immune response[345].
The adaptive immune response is characterized by the rapid and specific production of antibodies. The neutralizing IgM antibody is the first to be produced in the humoral response, peaking two weeks after vaccination and persisting for at least 18 months[344]. IgG antibodies are produced subsequently and can last up to 40 years in the body[252]. The vaccine provides effective immunity for 80%-100% of those vaccinated within 10 days and for over 99% within 30 days[254].
A randomized study conducted in Uganda demonstrated that a fractional dose (1/5 of the standard dose) was non-inferior to the standard dose in inducing seroconversion 28 days after vaccination[346]. These findings support the use of fractional doses during outbreaks when vaccine demand surges and in endemic regions where there is a shortage of YF vaccines.
According to WHO, people who are usually excluded from vaccination include[254]: (1) Infants aged less than 9 months; (2) Pregnant women-except during a YF outbreak when the risk of infection is high; (3) People with severe allergies to egg protein; and (4) People with severe immunodeficiency due to symptomatic HIV/AIDS or other causes, or who have a thymus disorder.
Despite the high reliability of the YF-17D vaccine, the occurrence of serious adverse events has been reported. These include vaccine-associated neurotropic disease, with a case fatality rate of 63%, and vaccine-associated viscerotropic disease, with a case fatality rate of less than 1.5%[241,344]. Additionally, anaphylaxis caused by the egg protein present in YF-17D vaccines is also a significant adverse effect[347].
The WHO recommends vaccination against YFV for travelers over nine months of age who are visiting areas at risk of YFV transmission. Additionally, with certain exceptions, vaccination is advised for all individuals residing in these regions, where it should be part of routine immunization programs. In the event of outbreaks, the WHO advocates for mass vaccination campaigns to achieve the necessary coverage to interrupt virus transmission[259] (Table 5).
| Intervention/treatment | ClinicalTrials.gov ID | Status | Phase | Sponsor |
| Biological: 17D Yellow fever vaccine | NCT05332197 | Unknown status | Phase 3 | London School of Hygiene and Tropical Medicine |
| Biological: STAMARIL®/biological: Yellow fever vaccine, bio-manguinhos/biological: yellow fever vaccine, institut pasteur/biological: Yellow fever vaccine, chumakov institute (fractional doses) | NCT02991495 | Completed | Phase 4 | Epicentre |
| Biological: Yellow fever vaccine, institut pasteur (fractional doses) | NCT04059471 | Completed | Phase 4 | University of Oxford |
| Biological: 17DD yellow fever vaccine | NCT02555072 | Completed | Phase 4 | The Immunobiological Technology Institute (Bio-Manguinhos)/Oswaldo Cruz Foundation (Fiocruz) |
| Biological: SII yellow fever vaccine/biological: STAMARIL® | NCT05421611 | Recruiting | Phase 3 | Serum Institute of India Pvt. Ltd. |
| Biological: 17D yellow fever vaccine/other: Deuterad water | NCT01290055 | Recruiting | Phase 4 | Sri Edupuganti |
| Biological: SII yellow fever vaccine/biological: STAMARIL® | NCT05447377 | Recruiting | Phase 3 | Serum Institute of India Pvt. Ltd. |
| Biological: 17DD yellow fever vaccine (fractional doses) | NCT03725618 | Unknown status | Phase 4 | Centers for Disease Control and Prevention |
| Biological: YF-VAX® | NCT00694655 | Recruiting | Phase 4 | Emory University |
| Placebo/biological: CYD tetravalent dengue vaccine/biological: STAMARIL® | NCT01436396 | Completed | Phase 3 | Sanofi Pasteur |
| Biological: YF-VAX® | NCT05374317 | Completed | Phase 4 | United States Army Medical Research Institute of Infectious Diseases |
| Biological: STAMARIL® | NCT01426243 | Completed | Phase 3 | French National Agency for Research on AIDS and Viral Hepatitis |
| Biological: Yellow fever vaccine/biological: MMR vaccine | NCT03368495 | Completed | Phase 4 | Alba Maria Ropero |
| Dietary supplement: vitamin A/biological: candidate plasmodium falciparum malaria vaccine/biological: MR-Vac/biological: STAMARIL® | NCT02699099 | Completed | Phase 3 | GlaxoSmithKline |
| Biological: 17 DD yellow fever vaccine, biomanguinhos | NCT03132311 | Recruiting | Phase 4 | Oswaldo Cruz Foundation |
| Biological: Typhoid Vi polysaccharide vaccine/biological: Yellow fever vaccine/biological: Japanese encephalitis vaccine/biological: Rabies Vaccine/biological: MenACWY-CRM vaccine | NCT01466387 | Completed | Phase 3 | Novartis |
| Placebo/TAK-003 tetravalent dengue vaccine/YF-17D yellow fever vaccine | NCT03342898 | Completed | Phase 3 | Takeda |
| Placebo/biological: BCG vaccine/biological: Yellow fever vaccine/drug: Vancomycin/drug: neomycin | NCT06148025 | Recruiting | Phase 4 | South Australian Health and Medical Research Institute |
CHIKV is a mosquito-borne virus responsible for periodic and explosive outbreaks of a febrile disease that is characterized by severe and sometimes prolonged polyarthritis[348]. CHIKV is in the Togaviridae family, genus Alphavirus. It is a small spherical enveloped virus, with a 60-70 nm diameter and its genome is a single strand RNA molecule of positive polarity, encoding four nonstructural (nsP1-4) and three structural proteins (C, E1, and E2)[349].
CHIKV is maintained in a complex sylvatic and rural cycle. The sylvatic cycles of CHIKV exist primarily in Africa between NHPs, rodents and possibly in bats and forest dwelling Ae. species (Ae. albopictus, Ae. furcifer, Ae. africanus, and Ae. taylori)[350]. Regarding rural and urban cycles, CHIKV transmission is primarily sustained within urban envi
Recent outbreaks of CHIKV in the Indian Ocean basin and Southeast Asia have been attributed to strains from the Indian Ocean lineage, a newly emerged subgroup within the ECSA clade[353]. This subgroup includes strains with an adaptive mutation (E1-A226V) that enhances viral fitness in Ae. albopictus mosquitoes, while maintaining replication efficiency in Ae. aegypti[354-357].
Thus, the intensification and expansion of vector-borne diseases are likely to become significant threats due to climate change. Although complicating factors such as mosquito range limits and viral evolution exist, climate change is expected to cause a substantial increase in exposure to Aedes-borne viruses. Moreover, several modeling studies predict that climate change will result in the expansion of vectors into temperate zones[358,359].
Despite the low mortality rates associated with CHIKV, it results in significant illness, severely affecting the quality of life for those affected and causing substantial economic losses, particularly in developing nations[360]. Recent outbreaks have heightened concerns about the potential public health impact of CHIKV in temperate regions. Factors such as urbanization, increased human mobility, viral adaptation, inadequate control measures, and the spread of new vectors are likely driving the resurgence of CHIKV infections[361].
CHIKV infection typically begins suddenly with a high fever, often accompanied by joint pain. Additional symptoms, though less common, can include severe polyarthralgia and arthritis, as well as rash, muscle pain, and headaches[348]. Acute symptomatic CHIKV disease often resembles other well-known arbovirus infections, such as DENV and ZIKV disease[362]. The simultaneous presence of these viruses in the same area complicates accurate diagnosis, as their symptoms can overlap and lead to frequent misdiagnoses.
Viral entry, replication and release: After the skin bite, the CHIKV enters subcutaneous capillaries and replicates in variety of susceptible cells, including dendritic cells, macrophages, synovial fibroblasts, ECs, and myocytes[362,363]. Additionally, it infects osteoblasts, contributing to the joint pathology and erosive disease observed in chronic arthritis patients[364]. To mediate the processes of entry and viral cell-cell spread, the fusion-related envelope glycoproteins of CHIKV, especially E1 and E2, expressed on the surface of the virion, are essential[365].
Thereby, multiple pathways and mechanisms are employed for CHIKV entry in a cell-type specific manner[366], such as then cell-adhesion molecule, matrix-remodeling-associated protein 8 (MXRA8), a multiple arthritogenic alphavirus receptor, widely expressed in epithelial and mesenchymal cells. Through the creation of various deletion variants, it has been demonstrated that the stalk region of MXRA8 is crucial for facilitating CHIKV entry as it binds in the ‘‘canyon’’ between two protomers of the E spike on the surface of the virion[365,367-369]. Besides, another host protein also identified as an entry factor for CHIKV is the CD147 complex, involved in its replication cycle. CD147 is widely expressed in various human cell types, including fibroblast and ECs. Interestingly, CD147 contains similar protein domains and high structural homology as the previously mentioned alphavirus entry factor MXRA8[370].
Glycosaminoglycans were also shown to be host molecules involved in the binding of CHIKV, particularly heparin/heparan sulfate[371,372]. Some of the other already know CHIKV cell receptors are prohibitin[373], the phospha
Furthermore, during the entry process, most reports indicate that CHIKV enters cells via clathrin-mediated endocytosis[377], although clathrin-independent pathways have been reported to mediate CHIKV entry to the target cells[378]. In addition, other pathways such as macropinocytosis[379,380], and the engulfment of apoptotic blebs[381]. Following entry, the virus’s incubation period ranges from three to seven days[362].
Upon the early endosome’s formation, clathrin molecules detach from the endocytic vesicle. This detachment, along with the endosome’s pH acidification, prompts the fusion of the endosomal membrane with the viral membranes (via the E1 protein), leading to the release of genomic RNA. Immediately following this release, the ribosome translates the non-structural polyproteins (P1234 precursor). Then, the P1234 polyprotein is cleaved by nsP2, liberating the individual non-structural proteins, which forms the viral replicase complex. Consequently, this complex mediates the synthesis of negative-strand RNA, which serves as templates for both new positive-strand RNA and 26S subgenomic RNA. Next, the synthesis of these RNA forms takes place in specialized replication compartments known as spherules. The subgenomic RNA is then translated into the structural polyprotein precursor C-pE2-6K-E1 in the rough ER. The C protein, containing a protease domain, self-cleaves, dissociates from the polyprotein, and assembles with the genomic RNA to form the icosahedral nucleocapsid core in the cytoplasm. The pE2-6K-E1 precursor is directed to the RER lumen for maturation, culminating in the formation of E1-E2 heterodimers. These heterodimers are inserted into the cell membrane, creating the “virus budding microdomain”. Finally, the assembled icosahedral nucleocapsid core migrates to this domain, where new viral particles are released extracellularly via the budding process[382-386].
Currently, the precise cellular mechanisms of the disease are still in need of elucidation. Although the structural details of the coat glycoproteins essential for viral entry are well understood, the potential target cell receptors and the exact mechanism of cell entry remain less well-known[387]. Lastly, numerous cell types, many of which are found at disease sites, are susceptible to CHIKV. As previously mentioned, these include chondrocytes, ECs, fibroblasts, hepatocytes, macrophages, monocytes, muscle satellite cells, myocytes, and osteoblasts[388-391].
Innate antiviral IFN response: Foremost, CHIKV infection induces systemic innate responses, primarily involving antiviral IFN-α, pro-inflammatory cytokines, and chemokines. This process is subsequently followed by the activation of adaptive immune responses[392].
When a chikungunya virion infects its initial target cells, it activates specific PRRs for RNA viruses, such as RLRs (RIG-I and MDA5) in the cytoplasm and TLRs, including TLR-3, TLR-7, and TLR-8 in the endosomal compartment[386,393]. This viral recognition initiates the signaling cascade of the innate immune response, activating IFN regulatory factors[394,395] and leading to the induction of type I-IFNs and various proinflammatory chemokines and cytokines. CHIKV infection has been demonstrated to induce the increased production of type I IFNs (IFN-α and IFN-β) as well as IFN-γ[394,396], that ultimately result in the induction of hundreds of ISGs that cooperatively establish an antiviral state within the infected and adjacent cells, including inhibition of viral replication and virion maturation[397-399].
Consequently, to persist within infected host cells, CHIKV has developed various strategies to evade IFN responses, much like many other viruses, such as CHIKV-encoded proteins strongly inhibiting the activation of the IFN-β and NF-κB promoters. Thus, CHIKV-encoded proteins may evade viral detection, resulting in a reduction of IFN responses[400-402].
Analysis of chemokines in CHIKV-infected patients shows a significant increase in IFN-γ-induced chemokines, such as CXCL9/MIG and CXCL10/IP-10, during the early days of infection[396]. IFN-γ, a primary cytokine for type 1 T helper cells, promotes the production of these chemokines, which are associated with the severity of CHIKV disease[403]. Additionally, elevated levels of CCL2/MCP-1, a known monocyte attractant, were detected, suggesting its involvement in disease progression and bone loss during chronic stages[404,405]. Furthermore, high levels of C5a anaphylatoxin were found early in the infection, a new observation. C5a’s role in inflammation, similar to its effects in rheumatoid arthritis and dengue fever, indicates its potential as a therapeutic target for managing rheumatic complications associated with CHIKV[406-408].
Adaptative immune response: There is relatively more knowledge about innate immune responses to infection, which primarily react to the acute phase of the disease[409]. Research indicates that CD4 T cells are essential for mediating humoral immunity against CHIKV[410]. In patients who have chronic chikungunya infection or have recovered from it, IFN-γ-producing CD4+ T and CD8+ T cells were detectable in the majority (85%) of the patients 12 to 24 months post-infection[392]. These T cells were primarily directed against the nsP1 and E2 peptides[411]. However, the pathogenic roles of CD4+ T cells have also been demonstrated, as findings indicate that CD4+ T, and not CD8+ T cells, are responsible for the joint inflammation induced by CHIKV infection[412].
In patients with acute CHIKV infection, CD8+ T cells were shown to be activated, evidenced by increased expression of activation markers such as CD69, CD107a, perforin, and granzyme, which suggests that CD8+ T cells are active during the acute phase and mediate cytotoxic activities[413]. Results such as the increased activation of CD8+ T cells in patients with acute CHIKV infection, the accumulation of CHIKV-specific CD8+ T cells in mouse spleen and joint-associated tissues, and their ability to produce IFN-γ upon ex vivo stimulation, suggest that CD8+ T cells are functionally active during the acute phase[414]. However, the fact that these effector T cells did not reduce viremia levels, combined with the observation that pre-existing functional effector CD8+ T cells led to CHIKV clearance mainly in the spleen, suggests that CHIKV has developed strategies to evade CD8+ T cell recognition, allowing it to establish chronic infection in the joints[414].
Antibodies play a crucial role in controlling CHIKV infection[410]. Anti-CHIKV IgM levels gradually increase from as early as day 2-4 after symptom onset[415,416] and then remain stable for up to 4 months[417]. Similarly, anti-CHIKV IgG can be detected in the early convalescent stage, appearing around 10 days post-symptom onset in some patients, and persists for 2-3 months[418]. Early formation of IgG3 antibodies at day 10 correlates with reduced viremia levels and mitigates chronic and severe disease[418]. Moreover, early production of IgM antibodies, which possess neutralizing capabilities, contributes to lowering viremia levels, and the neutralizing activity of IgM complements early IgG antibodies and plays a critical role from days 4 to 10 post-symptom onset[416]. Additionally, the presence of both IgM and IgG is associated with modulation of cytokine and chemokine levels, suggesting their role in regulating immune responses in CHIKV-infected patients[418,419].
Antibodies directed against the E2 glycoprotein are critical in the immune response to CHIKV infection[410,420-422]. Furthermore, studies in CHIKV-infected patients have identified several monoclonal antibodies that neutralize the virus by targeting epitopes in the E1 and E2 glycoproteins, with E2-specific antibodies proving effective in protecting against lethal chikungunya infection[423]. These antibodies block viral fusion and release from infected cells[420]. Moreover, analysis of antibody responses in patients has revealed that CHIKV-specific IgG avidity increases over time, correlating with improved neutralizing capacity[414]. Additionally, patients in the acute phase show higher avidity against E1 and E2 proteins compared to those with chronic infections[424], suggesting that robust antibody responses may play a crucial role in preventing chronic disease progression.
Chronic chikungunya arthritis: It is roughly estimated that 30% to 40% of infected individuals experience some long-term sequelae. These sequelae include persistent arthralgia and/or arthritis, with severe pain present in about 37% of individuals suffering from persistent arthralgia[425]. Factors associated with the persistence of arthralgia in CHIKV-infected patients have not been fully explored. However, the few available studies indicate that patients over 40 years old, females, and those with higher levels of CXCL8 detected during the acute phase of the disease are more likely to experience persistent arthralgia[426,427].
Recent studies have identified human synovial tissues as sanctuaries for CHIKV, where viral RNA persists in joint fluid[428]. This persistence is thought to contribute to CHIKV -associated arthritis by infecting fibroblast-like synoviocytes and promoting the migration of primary human monocytes[429]. These monocytes/macrophages can then transform into osteoclast-like cells, producing high levels of TNF-α and IL-6 proinflammatory cytokines.
Despite advancements in our understanding of CHIKV infection, the exact immunopathogenic mechanisms that lead to CHIKV-induced arthralgia remain unclear. Cytokines and chemokines are key players in CHIKV immunopathology, considering that during the early acute phase, serum proinflammatory cytokines such as IFN-α, IFN-β, IFN-γ, CXCL10/IP-10, and IL-1β show a strong upregulation. IFN-α is detected early during infection, often on the first day, and its concentration correlates with viral load, which is significantly higher in elderly patients[430]. Additionally, the elevation of MCP-1, IL-6, IL-8, MIP-1α, and MIP-1β is most prominent in the chronic phase[431].
Furthermore, another study found that levels of CXCL9/MIG and CXCL10/IP-10, along with high concentrations of IgG, were associated with severe symptoms in CHIKV patients[432]. Moreover, TNF-α and IFN-γ-secreting NK-like T cells were elevated in patients with persistent CHIKV arthralgia[433]. In addition, a systematic meta-analysis of immune signatures in patients with acute CHIKV infection showed a correlation between increased proinflammatory cytokines and arthralgia[426].
CHIKV infection is typically classified into three stages: The acute stage (lasting from day 1 to day 21), the post-acute stage (spanning from day 21 to 3 months), and the chronic stage (lasting beyond 3 months)[434].
Acute phase of infection: During the acute stage, infected patients may undergo a viremic phase lasting 5 to 10 days, followed by a post-viremic phase lasting 6 to 21 days[434]. The acute viremic stage of CHIKV infection is characterized by an abrupt onset of high-grade fever (often > 39 °C), arthralgia, myalgia, headache, fatigue, nausea, vomiting, and arthritis. Additionally, other symptoms such as conjunctivitis, exanthema, and edema may also occur. The exanthema can manifest as a diffuse or focal skin rash. Despite these symptoms, the disease is self-limiting, and in most patients, it resolves within 7-10 days[430,435].
In the post-acute phase, symptoms exhibit diverse manifestations stemming from persistent initial acute symptoms, such as joint issues and fatigue, while fever typically subsides[436]. Additionally, polyarthritis tends to affect both sides of the body symmetrically, involving both small and large joints like knees, ankles, hands, and wrists and there may be periarticular involvement, including enthesitis, tenosynovitis, and bursitis[437,438]. Furthermore, acute CHIKV infection can potentially exacerbate pre-existing autoimmune arthritis[439].
Severe symptoms affecting vital organs can develop during CHIKV infection, including encephalitis, encephalopathy, and neuro-ocular diseases (such as uveitis, retinitis, and optic neuritis), as well as myelopathy and myelitis, Guillain-Barré syndrome, myocarditis, hepatitis, acute interstitial nephritis, severe sepsis, septic shock, and multi-organ failure[440-442]. Furthermore, individuals with comorbidities, the elderly, and infants are at a higher risk for these severe symptoms[442-444]. Additionally, perinatal CHIKV infection can result in sequelae such as microcephaly, cerebral palsy, and neurocognitive impairment[445].
Chronic or persistent phase of infection: The chronic stage of CHIKV infection is marked by symptoms that persist for over three months following the initial diagnosis of acute infection. Specifically, this chronic phase often affects distal joints due to continuous viral replication and inflammation. Moreover, the virus has been detected in several organs, including ECs in the liver, mononuclear cells in the spleen, macrophages in the synovial fluid and surrounding tissues, and satellite cells in the muscles[348].
During the chronic stage, patients can suffer from unpredictable relapses of fever, fatigue, joint pain, and stiffness[446,447]. Furthermore, older individuals and those with a history of rheumatic or traumatic joint disorders are more likely to develop this chronic phase[447]. Age, female sex, and dehydration state during the acute phase are also important factors[448].
Diagnosis: The diagnosis of CHIKV infection can be conducted using various methods, including viral isolation, serological assays, and RNA detection through real-time quantitative reverse transcriptase PCR (qRT-PCR)[449]. RT-PCR and virus isolation are most effective when conducted near the onset of febrile illness, when viremia is at its peak. Serological tests to detect IgM and IgG antibodies are best performed approximately seven days after the onset of symptoms[386].
Diagnosing CHIKV infection solely based on clinical symptoms poses significant challenges, particularly in endemic regions where other arboviruses like DENV and ZIKV are also circulating. Healthcare providers should consider CHIKV infection in patients exhibiting acute febrile illness and polyarthralgia, especially among travelers returning from areas known for CHIKV transmission[386].
Virus isolation through cell culture is considered the gold standard for viral detection due to its high specificity[447]. To isolate CHIKV, various cell lines from humans, monkeys, and mosquitoes have been utilized[450]. CHIKV infection typically results in a noticeable CPE in culture, which can be observed as early as 24 hours after infection[363].
Nucleic acid detection is a rapid and highly sensitive assay used to diagnose CHIKV infection. One common method is qRT-PCR, which detects the CHIKV genome[451-454]. This technique can also be employed in multiplex PCR assays to simultaneously detect other arboviruses, including ZIKV[454]. A conserved region of the envelope E1 and E2 genes is the most common target for qRT-PCR, and other targets include nsP1 and nsP4 genes[451,452,455]. The viral RNA of CHIKV can be detected by the qRT-PCR method from 0 to 7 days of infection, after which qRT-PCR detection becomes unreliable[456].
Serological testing, simpler than qRT-PCR, can detect anti-CHIKV immunoglobulin M (IgM) and IgG. These antibodies are detectable using ELISA, immunofluorescence assays (IFA), and PRNT[457]. Among these, IgM ELISA is the most frequently utilized method for diagnosing CHIKV infection[458]. Serology-based diagnosis is constrained by potential cross-reactivity with other arboviruses[459]. CHIKV shares antigenic similarities with other viruses in the Alphavirus genus, such as Semliki forest virus, Mayaro virus, and o’nyong nyong virus[460].
A systematic review and meta-analysis found that IgM detection tests demonstrated over 90% diagnostic accuracy for ELISA-based tests, IFA, in-house developed tests, and samples collected more than seven days after symptom onset. However, sensitivity was lower for rapid tests (42.3%), commercial tests (78.6%), and samples collected within seven days before symptom onset (26.2%). Therefore, IgM detection tests are particularly recommended for use with samples obtained during the convalescent phase of CHIKV infection. The specificity of IgM detection tests remained above 90% across all test formats and sample collection times[461].
Serological tests for CHIKV E1/E2 antigen detection, including rapid assays[461,462], ELISA-based tests[456], and FLISA-based tests[458] have shown promising performance. However, challenges in developing antigen-based tests include variability in performance across different CHIKV genotypes[463]. Therefore, further evaluation in diverse geographical settings is crucial to validate these tests against all circulating CHIKV genotypes.
Treatment: At present, treatment for chikungunya primarily aims to alleviate symptoms, as there is no dedicated vaccine or specific treatment available. As a result, a range of drugs have been utilized with mixed effectiveness, primarily targeting supportive care and the reduction of joint pain. It should be tailored to the clinical context and targeted at specific risk groups, focusing on managing fever and pain, addressing dehydration, providing organ support, and preventing iatrogenic complications and functional impairment[464]. Key pharmaceutical treatments for chikungunya include NSAIDs, disease-modifying antirheumatic drugs, and antivirals[465].
Analgesia using acetaminophen is the preferred treatment. Avoiding NSAIDs and salicylates within the initial 14 days of disease onset is advised due to the risk of bleeding complications associated with dengue fever, unless dengue has been definitively ruled out[464]. No specific NSAID class has demonstrated superiority in effectively managing post-chikungunya symptoms. In cases where conditions such as tenosynovitis, bursitis, tunnel syndrome, capsulitis, or synovitis are not adequately controlled by oral treatments, local anti-inflammatory therapy (either topical or via infiltration) should be prescribed to minimize excessive systemic medication use[434].
The use of corticosteroids is not recommended due to the risk of severe rebound arthritis and tenosynovitis. Therefore, systemic corticosteroids should only be considered for treating inflammatory polyarticular presentations, particularly when there is concurrent tenosynovitis or active synovitis, or when NSAIDs are ineffective or contraindicated[460].
In animal models of CHIKV infection, the use of CHIKV IgG or CHIKV-specific monoclonal antibodies for prophylaxis has demonstrated protective effects[466]. This highlights the potential of antibody-based therapies as a promising strategy for preventing severe CHIKV infection in at-risk individuals.
In cell-based screenings aimed at combating CHIKV infection, several drugs with antiviral properties have been identified. These drugs target distinct stages of the CHIKV replication cycle: Chloroquine[467] and chlorpromazine[468] act on virus entry, while harringtonine and homoharringtonine[469] affect viral protein translation. Others, such as trigocherriolide A[470], ribavirin[471], IFN-alpha[472], apigenin, and silybin[468], and inhibit virus replication.
Vaccines: Given the rapid spread of CHIKV across many countries, vaccinating the susceptible population remains the most effective method to control infection. CHIKV preclinical candidate vaccines under development encompass a variety of approaches, including a whole-virus inactivated vaccine[473], a VEE/CHIKV chimeric vaccine[474], a re
| Vaccine technology platforms | Intervention/treatment | ClinicalTrials.gov ID | Phase | Status | Sponsor |
| Virus-like particle vaccine | Biological: VRC-CHKVLP059-00-VP | NCT01489358 | 1 | Completed | NIAID |
| Biological: PXVX0317 | NCT03992872 | 2 | Completed | Bavarian Nordic | |
| Biological: CHIKV VLP/adjuvant | NCT05072080 | 3 | Completed | Bavarian Nordic | |
| Biological: VRC-CHKVLP059-00-VP | NCT02562482 | 2 | Completed | NIAID | |
| Viral vectored vaccine | Biological: MV-CHIK/ Biological: MMR-vaccine | NCT03101111 | 2 | Completed | Themis Bioscience GmbH |
| Biological: ChAdOx1 Chik | NCT04440774 | 1 | Completed | University of Oxford | |
| Live attenuated vaccine | Biological: VLA1553 | NCT04650399 | 3 | Completed | Butantan Institute |
| Biological: VLA1553 | NCT03382964 | 1 | Completed | Valneva Austria GmbH | |
| Biological: V184 | NCT03807843 | 2 | Completed | Themis Bioscience GmbH | |
| Inactivated whole virion vaccine | Biological: BBV87 | NCT04566484 | 3 | Completed | International Vaccine Institute |
The leading vaccine candidate, a live-attenuated Δ5nsP3 (Valneva), has successfully completed Phase III trials and is now in the process of obtaining licensure. This vaccine stands out due to its superiority over single-dose regimens, achieving a remarkable 98.9% seroconversion in adults and older adults. It holds potential benefits for travelers planning to visit endemic areas. Nevertheless, further research is needed to determine its effectiveness in providing protection within endemic regions[479-481].
Another vaccine candidate, the adjuvanted VLP (CHIKV VLP) PXVX0317PXV, is non-self-replicating and known for its ability to elicit robust immunogenicity. However, it necessitates two doses, and the ongoing trial does not include participants from endemic areas. Therefore, this vaccine might be a viable option for immunocompromised individuals[482-485].
In summary, DENV, ZIKV, YFV, and CHIKV share several common characteristics, including their protein structure, tropism, evasion of the immune response, and various symptoms such as fever and rash. Moreover, they often have common transmission vectors and can exhibit cross-reactions in laboratory tests. Nonetheless, their individualities can significantly aid in differential diagnosis, necessitating healthcare professionals to adopt a clinical management approach tailored to the patients’ symptoms and to prevent potential complications typically associated with a specific virus. For example, dengue is often correlated with hemorrhages, Zika with microcephaly, YFV with hepatitis, and CHIKV with polyarthralgia.
However, it is essential to highlight that the immune response of each patient and their symptoms are not always clear, and symptoms more commonly associated with one viral infection can also be present in others. Therefore, laboratory and epidemiological diagnoses, considering local endemics and current outbreaks, are crucial in accurately diagnosing the aforementioned arboviruses.
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