• HIV
• Inflammatory bowel disease
• Systematic review and meta-analysis

• Humans
• HIV Infections/epidemiology
• Inflammatory Bowel Diseases/epidemiology
• Odds Ratio
• Risk Factors

• 2019C03076 the Key Research Project of Zhejiang Province for Traditional Chinese Medicine
• 2023YFC3603100 and 2023YFC3603105 the National Key Research and Development Program of China
• 2022C03076-4 "Leading Goose" R&D Program of Zhejiang
• “Leading Goose” R&D Program of Zhejiang

• Idiopathic thrombocytopenic purpura
• Metabolome
• Microbiota
• Prognosis
• Therapeutics

• Humans
• Dysbiosis/microbiology
• Gastrointestinal Microbiome
• Purpura, Thrombocytopenic, Idiopathic/microbiology
• Purpura, Thrombocytopenic, Idiopathic/etiology
• Purpura, Thrombocytopenic, Idiopathic/diagnosis
• Purpura, Thrombocytopenic, Idiopathic/immunology

• Immune thrombocytopenia (ITP)
• Immunomodulation
• Pathophysiology
• Remission
• Romiplostim
• Therapy free remission

• Humans
• Receptors, Fc/therapeutic use
• Thrombopoietin/therapeutic use
• Recombinant Fusion Proteins/therapeutic use
• Purpura, Thrombocytopenic, Idiopathic/drug therapy
• Receptors, Thrombopoietin/agonists

• C-reactive protein
• Immune thrombocytopenia purpura
• Platelet
• Prognosis

• Adult
• Humans
• C-Reactive Protein
• Prognosis
• Purpura, Thrombocytopenic, Idiopathic/diagnosis
• Retrospective Studies
• Thrombocytopenia

• 82070127 National Natural Science Foundation of China

Primary immune thrombocytopenia (ITP) is an autoimmune disease. Some ITP patients are associated with pathogen infection undetected with conventional technologies. Investigating the changes of T cells and potential metabolic mechanism are important for better understanding of ITP.

The study enrolled 75 newly diagnosed ITP patients. The pathogens of patients were detected by metagenomic next-generation sequencing (mNGS). Plasma lipids were measured by liquid chromatography-mass spectrometry (LC–MS). CD4 T cell and CD8 T cell were analyzed using flow cytometry. Mitochondrial reactive oxygen species (ROS) and mitochondrial membrane potential were measured by flow cytometry. Seahorse XF real-time ATP rate assay was used to investigate the change of cellular metabolism.

Positive plasma pathogens were detected in seven ITP patients. Of them, 5 (71.4%) positive pathogen-ITP patients were no response (NR) after first-line treatment with corticosteroids. Regulatory T cells (Tregs) increased significantly in positive pathogen-ITP patients compared to negative pathogen-ITP patients and healthy controls (HC). Mitochondrial membrane potential of Th17 and Tregs were decreased in positive pathogen-ITP and negative pathogen-ITP patients, compared to HC (all p < 0.05). The overall metabolism flux of positive pathogen-ITP patients was decreased, as compared to HC (p = 0.004), of them a higher proportion of glycolysis-derived ATP and a smaller proportion of oxidative phosphorylation (OXPHOS)-derived ATP were found in Tregs. The ATP rate index of Tregs was decreased significantly in positive pathogen-ITP patients compared to negative pathogen-ITP patients and HC (p < 0.05).

Impaired mitochondria function of Tregs in positive pathogen-ITP patients caused a decrease of OXPHOS-derived ATP and overall metabolism flux that might be the cause of steroid resistance in ITP patients.

• Glycolysis
• Immune thrombocytopenia
• Oxidative phosphorylation
• Pathogens
• Tregs (Regulatory T cells)

• Humans
• Uveomeningoencephalitic Syndrome/complications
• Uveomeningoencephalitic Syndrome/diagnosis
• Uveomeningoencephalitic Syndrome/drug therapy
• HIV Infections/complications
• HIV Infections/diagnosis

In people living with the human immunodeficiency virus, haematological abnormalities have been linked to an increased risk of disease progression and mortality. Hematological parameters may have a positive or negative impact on antiretroviral therapy. The aim of this study was to assess the immuno-haematological abnormalities of HIV-infected patients before and after the initiation of highly active antiretroviral therapy in the antiretroviral therapy clinics of six health facilities in Dessie, Northeast Ethiopia.

A facility-based cross-sectional study was conducted from April to May 30, 2021, at the antiretroviral therapy clinics of six health facilities in Dessie Town. A total of 378 HIV-infected patients taking highly active antiretroviral treatment for at least 6 months by using a consecutive sampling technique were included. A well-organized questionnaire was used to collect socio-demographic and clinical information. Immune-haematological parameters were tested using a Mindray BS-300 hematology analyzer and a BD FACS count CD4 analyzer. Statistical analysis was performed using SPSS version 25 statistical software. Statistical significance was defined as a P-value of 0.05 with a 95% confidence interval.

Leukopenia was found in 26.7% and 16.5%, neutropenia in 16.5% and 9.4%, lymphopenia in 20% and 3.1%, and thrombocytopenia in 25.9% and 7.1% of HIV patients before and after HAART initiation, respectively. There was a significant difference in total white blood cell, absolute neutrophil, red blood cell, hemoglobin value, mean cell volume, mean cell haemoglobin, mean cell haemoglobin concentration, red cell distribution width, platelet and CD4+ T cell counts in HIV patients before and after the initiation of HAART with P < 0.05.

Anemia, leukopenia, neutropenia, lymphopenia, and thrombocytopenia were the most common haematological abnormalities found in this study before and after HAART initiation. The prevalence of thrombocytopenia, immunosuppression, and viral load was reduced considerably after starting HAART.

Immune thrombocytopenia (ITP) may occur in isolation (primary) or in association with a predisposing condition (secondary ITP [sITP]). Eltrombopag is a well-studied treatment for primary ITP, but evidence is scarce for sITP. We evaluated real-world use of eltrombopag for sITP using electronic health records. Eligible patients had diagnoses of ITP and a qualifying predisposing condition, and eltrombopag treatment. We described patient characteristics, treatment patterns, platelet counts, and thrombotic and bleeding events. We identified 242 eligible patients; the most common predisposing conditions were hepatitis C and systemic lupus erythematosus. Average duration of eltrombopag treatment was 6.1 months. Most (81.4%) patients achieved a platelet count ≥ 30,000/µL at a mean of 0.70 months, 70.2% reached ≥ 50,000/µL at a mean of 0.95 months, and 47.1% achieved a complete response of > 100,000/µL at a mean of 1.43 months after eltrombopag initiation. At eltrombopag discontinuation, 105 patients (43%) experienced a treatment-free period for a mean 3.3 months. Bleeding events occurred with similar frequency before and during eltrombopag treatment whereas thrombotic events were less frequent during eltrombopag treatment. Our results suggest similar rates of platelet response with eltrombopag in patients with sITP as compared with primary ITP. In addition, a treatment-free period is possible for a substantial minority of patients.

• Electronic health records
• Eltrombopag
• Platelet response
• Retrospective study
• Secondary immune thrombocytopenia

HIV infection has been associated with a non-erosive inflammatory arthritis in children, although few published reports exist. This study describes the clinical, laboratory and imaging features of this noncommunicable disease in a series of HIV-infected children in South Africa.

A database search was conducted to identify HIV-infected children enrolled in a Paediatric Rheumatology service in Cape Town, South Africa between 1 January 2010 and 31 December 2020. Retrospective data were collected from individuals classified with HIV arthropathy, based on a predefined checklist. Demographic, clinical, laboratory, sonographic, therapeutic, and outcomes data were extracted by chart review. Descriptive statistical analysis was performed using R (v4.0.3).

Eleven cases of HIV arthropathy were included in the analysis. Cases predominantly presented in older boys with low CD4+ counts. Median age at arthritis onset was 10.3 years (IQR 6.9 – 11.6) and the male-female ratio was 3.0. The median absolute CD4+ count was 389 cells/uL (IQR 322 – 449). The clinical presentation was variable, with both oligoarthritis and polyarthritis being common. Elevated acute phase reactants were the most consistent laboratory feature, with a median ESR of 126 mL/h (IQR 67 – 136) and median CRP of 36 mg/L (IQR 25 – 68). Ultrasonography demonstrated joint effusions and synovial hypertrophy. Response to therapy was slower than has generally been described in adults, with almost all cases requiring more than one immunosuppressive agent. Five children were discharged in established remission after discontinuing immunotherapy, however outcomes data were incomplete for the remaining six cases.

In this case series, HIV arthropathy was associated with advanced immunosuppression. Therapeutic modalities included immunomodulators and antiretroviral therapy, which consistently induced disease remission although data were limited by a high rate of attrition. Prospective studies are needed to define and understand this HIV-associated noncommunicable disease.

• Africa
• autoimmunity
• inflammatory arthritis
• musculoskeletal manifestations
• non-communicable disease
• paediatric HIV

A 35-year-old male was referred to our hospital with dysesthesia of the lower extremities that had begun six months earlier. A blood test revealed the presence of various antibodies, suggesting a collagen-related peripheral neuropathy. However, a history of repeated shingles and sex with males was noted, and the patient was tested for and diagnosed with human immunodeficiency virus (HIV) infection. Based on the manifestations and laboratory data, including the results of immunological and urinary tests, he was further diagnosed with concomitant systemic lupus erythematosus (SLE). The activity of SLE improved with antiretroviral therapy. There is currently no established treatment for AIDS complicated with SLE. Indeed, because HIV treatment involves the activation of immune function and SLE treatment involves immunosuppression, any treatments for the two conditions would be in conflict. It is thus necessary to select a treatment strategy based on the condition of the individual patient. In addition, because HIV infection is relatively rare in Japan compared to other countries, rheumatologists in Japan must keep HIV infection in mind as a differential diagnosis for autoimmune diseases.

• acquired immunodeficiency syndrome
• antiretroviral therapy
• autoimmune disease
• human immunodeficiency virus
• systemic lupus erythematosus

Hematological abnormalities have been associated with an increased risk of disease progression and death in people living with human immunodeficiency virus (HIV). The use of antiretroviral medications can have a positive or negative effect on the hematological disorder. However, little is known about its impact on hematological parameters in antiretroviral-treated patients in Ethiopia, especially in the study area.

A cross-sectional study was conducted at Debre Tabor Comprehensive Specialized Hospital from September to November 2020. A total of 334 HIV-infected patients taking highly active antiretroviral treatment (HAART) at least for 6 months were selected using a simple random sampling technique. Socio-demographic and clinical characteristics of the study subjects were collected using a semi-structured questionnaire. Hematological and immunological parameters were determined using Sysmex kx-21 hematology analyzer and BD FACS count CD4 analyzer, respectively. Statistical analysis was done using SPSS version 20 statistical software. A P-value <0.05 was considered statistically significant.

A total of 334 HIV patients were included in this study. The prevalence of anemia, leucopenia, neutropenia, lymphopenia and thrombocytopenia were 37.1%, 22.8%, 8.4%, 10.5% and 17.1% before initiation of HAART and 17.4%, 34.2%, 18.8%, 13.1% and 8.3% after initiation of HAART, respectively. There was a significant difference in total white blood cell (WBC) count, absolute neutrophil count (ANC), red blood cell (RBC) count, hemoglobin value, mean cell volume (MCV), mean cell hemoglobin (MCH), mean cell hemoglobin concentration (MCHC), red cell distribution width (RDW), platelet and CD4+ T cell counts in HIV patients before and after initiation of HAART (P<0.05).

The most common hematological abnormalities observed in this study before and after HAART initiation were anemia, leucopenia, neutropenia, lymphopenia, and thrombocytopenia. However, after beginning HAART, the prevalence of anemia and thrombocytopenia decreased dramatically.

• HAART
• HIV
• anemia
• leucopenia
• thrombocytopenia

• COVID-19
• host immune responses
• microbial pathogens
• platelets
• thrombosis

• Adaptive Immunity
• Betacoronavirus
• Blood Platelets/immunology
• Blood Platelets/metabolism
• COVID-19
• Coronavirus Infections/immunology
• Coronavirus Infections/virology
• Hemostasis
• Host-Pathogen Interactions/immunology
• Humans
• Immunity, Innate
• Inflammation/immunology
• Pandemics
• Pneumonia, Viral/immunology
• Pneumonia, Viral/virology
• SARS-CoV-2
• Thrombosis/metabolism

• CIHR

• CCR2
• CCR5
• HIV
• cenicriviroc
• fibrosis

• ITP
• diagnosis
• physiopathology
• pregnancy
• treatment

• AIDS
• CD4 counts
• HIV
• Hematologic abnormality
• anemia

• HAART
• HIV
• anemia
• prevalence
• thrombocytopenia

Immune thrombocytopenia (ITP) is an autoimmune disease defined by low platelet counts which presents with an increased bleeding risk. Several genetic risk factors (e.g., polymorphisms in immunity-related genes) predispose to ITP. Autoantibodies and cytotoxic CD8⁺ T cells (Tc) mediate the anti-platelet response leading to thrombocytopenia. Both effector arms enhance platelet clearance through phagocytosis by splenic macrophages or dendritic cells and by induction of apoptosis. Meanwhile, platelet production is inhibited by CD8⁺ Tc targeting megakaryocytes in the bone marrow. CD4⁺ T helper cells are important for B cell differentiation into autoantibody secreting plasma cells. Regulatory Tc are essential to secure immune tolerance, and reduced levels have been implicated in the development of ITP. Both Fcγ-receptor-dependent and -independent pathways are involved in the etiology of ITP. In this review, we present a simplified model for the pathogenesis of ITP, in which exposure of platelet surface antigens and a loss of tolerance are required for development of chronic anti-platelet responses. We also suggest that infections may comprise an important trigger for the development of auto-immunity against platelets in ITP. Post-translational modification of autoantigens has been firmly implicated in the development of autoimmune disorders like rheumatoid arthritis and type 1 diabetes. Based on these findings, we propose that post-translational modifications of platelet antigens may also contribute to the pathogenesis of ITP.

• CD8+ T cells
• ITP
• autoantibodies
• autoimmunity
• immune thrombocytopenia
• immune thrombocytopenic purpura

• acquired immunodeficiency syndrome
• antigenic mimicry
• autoholoimmunity
• autoimmunity
• holoimmunity
• lymphocytotoxic autoantibodies
• microbiome
• tolerance

• Acquired Immunodeficiency Syndrome/immunology
• Acquired Immunodeficiency Syndrome/virology
• Animals
• Autoimmunity
• Cross Reactions
• HIV/chemistry
• HIV/immunology
• Human Immunodeficiency Virus Proteins/chemistry
• Human Immunodeficiency Virus Proteins/immunology
• Humans
• Microbiota
• Molecular Mimicry
• Proteomics
• Receptors, Antigen, T-Cell/chemistry
• Receptors, Antigen, T-Cell/immunology

• C-reactive protein
• antiplatelet antibodies
• immune thrombocytopenic purpura

Multiple sclerosis (MS) is an autoimmune chronic inflammatory disease of the central nervous system (CNS). Cross-reactivity of neuronal proteins with exogenous antigens is considered one of the possible mechanisms of MS triggering. Previously, we showed that monoclonal myelin basic protein (MBP)-specific antibodies from MS patients cross-react with Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1). In this study, we report that exposure of mice to LMP1 results in induction of myelin-reactive autoantibodies in vivo. We posit that chronic exposure or multiple acute exposures to viral antigen may redirect B cells from production of antiviral antibodies to antibodies, specific to myelin antigen. However, even in inbred animals, which are almost identical in terms of their genomes, such an effect is only observed in 20–50% of animals, indicating that this change occurs by chance, rather than systematically. Cross-immunoprecipitation analysis showed that only part of anti-MBP antibodies from LMP1-immunized mice might simultaneously bind LMP1. In contrast, the majority of anti-LMP1 antibodies from MBP-immunized mice bind MBP. De novo sequencing of anti-LMP1 and anti-MBP antibodies by mass spectrometry demonstrated enhanced clonal diversity in LMP1-immunized mice in comparison with MBP-immunized mice. We suggest that induction of MBP-reactive antibodies in LMP1-immunized mice may be caused by either Follicular dendritic cells (FDCs) or by T cells that are primed by myelin antigens directly in CNS. Our findings help to elucidate the still enigmatic link between EBV infection and MS development, suggesting that myelin-reactive antibodies raised as a response toward EBV protein LMP1 are not truly cross-reactive but are primarily caused by epitope spreading.

• Epstein–Barr virus
• autoantibodies
• cross-reactivity
• epitope spreading
• latent membrane protein 1
• multiple sclerosis
• myelin basic protein

• Extended phenotype
• Glanzmann thrombasthenia
• Inflammation and immunity
• Inherited platelet disorder
• Thrombosis and cancer
• β3-Integrins

• Animals
• Blood Coagulation
• Blood Platelets/metabolism
• Cardiovascular Diseases/blood
• Cardiovascular Diseases/diagnosis
• Cardiovascular Diseases/etiology
• Cardiovascular Diseases/metabolism
• Disease Susceptibility
• Fibrinolysis
• Genetic Association Studies
• Genotype
• Humans
• Integrin alphaVbeta3/genetics
• Integrin alphaVbeta3/metabolism
• Mutation
• Phenotype
• Platelet Glycoprotein GPIIb-IIIa Complex/genetics
• Platelet Glycoprotein GPIIb-IIIa Complex/metabolism
• Polymorphism, Genetic
• Thrombasthenia/blood
• Thrombasthenia/complications
• Thrombasthenia/genetics

• Autoimmune Diseases
• Infections
• T Cells

• Acquired Immunodeficiency Syndrome/drug therapy
• Adult
• Anemia, Hemolytic, Autoimmune/epidemiology
• Antiretroviral Therapy, Highly Active
• Autoimmune Diseases/epidemiology
• Female
• Humans
• Incidence
• Lupus Erythematosus, Systemic/epidemiology
• Male
• Psoriasis/epidemiology
• Sex Factors
• Sjogren's Syndrome/epidemiology
• Spondylitis, Ankylosing/epidemiology
• Taiwan/epidemiology
• Uveitis/epidemiology
• Young Adult

AIDS, caused by HIV, is a multisystem disease that affects hematopoiesis. The aim of this study was to assess cytopenias among HIV-infected children who had a follow-up at Felege Hiwot Referral Hospital, Bahir Dar, northwest Ethiopia.

An institution-based cross-sectional study was conducted between April and May 2013. Systematic random sampling method was used to select the study participants. Descriptive statistics, independent t-test as well as chi-square and logistic regression were used for analysis. A p-value <0.05 was considered as statistically significant.

A total of 224 children (112 highly active antiretroviral therapy [HAART]-naïve and 112 HAART-experienced) participated in the study. The magnitude of anemia, thrombocytopenia, neutropenia, leukopenia and pancytopenia among HAART-naïve HIV-infected children were 30.4%, 9.8%, 8%, 4.5% and 1.8%, respectively. The overall prevalence of anemia, neutropenia, thrombocytopenia, leukopenia and pancytopenia were 29.5%, 8.9%, 8%, 4.5% and 1.4%, respectively. Cluster of differentiation-4 percentage and mean corpuscular volume were significantly different between HAART-experienced and HAART-naïve children. Being of younger age and severely immunosuppressed were risk factors of anemia.

Anemia was the most common cytopenia, followed by neutropenia. Severe immunosuppression and younger age were significantly associated with anemia. Therefore, emphasis should be given for investigation and management of cytopenias in HIV-infected children, particularly for those who are immunosuppressed and of younger age.

• HAART
• HIV
• anemia
• children
• cytopenia
• leukopenia
• neutropenia
• pancytopenia
• thrombocytopenia

Virus–platelet interplay is complex. Diverse virus types have been shown to associate with numerous distinct platelet receptors. This association can benefit the virus or the host, and thus the platelet is somewhat of a renegade. Evidence is accumulating to suggest that viruses are capable of entering platelets. For at least one type of RNA virus (dengue virus), the platelet has the necessary post-translational and packaging machinery required for production of replicative viral progeny. As a facilitator of immunity, the platelet also participates in eradicating the virus by direct and indirect mechanisms involving presentation of the pathogen to the innate and adaptive immune systems, thus enhancing inflammation by release of cytokines and other agonists. Virus-induced thrombocytopenia is caused by tangential imbalance of thrombopoeisis, autoimmunity, and loss of platelet function and integrity.

• respiratory syncytial virus
• protein disulfide isomerase
• hemorrhagic fever
• denv infection
• human brain microvascular endothelial cell

Immune thrombocytopenia (ITP) is a complex autoimmune disease characterized by low platelet counts. The pathogenesis of ITP remains unclear although both antibody-mediated and/or T cell-mediated platelet destruction are key processes. In addition, impairment of T cells, cytokine imbalances, and the contribution of the bone marrow niche have now been recognized to be important. Treatment strategies are aimed at the restoration of platelet counts compatible with adequate hemostasis rather than achieving physiological platelet counts. The first line treatments focus on the inhibition of autoantibody production and platelet degradation, whereas second-line treatments include immunosuppressive drugs, such as Rituximab, and splenectomy. Finally, third-line treatments aim to stimulate platelet production by megakaryocytes. This review discusses the pathophysiology of ITP and how the different treatment modalities affect the pathogenic mechanisms.

• immune thrombocytopenia (ITP)
• B cells
• T cells
• autoimmunity
• platelets

• HCV
• HIV
• Helicobacter pylori
• Infections
• thrombocytopenia

• Chemokines
• Cytokines
• Immunity
• Infections
• Inflammation
• Platelets

• HIV infection
• benign haematological complications
• coagulation
• pancytopenia

We aimed to determine the prevalence and correlates of thrombocytopenia among people living with human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS) and to assess occurrence of antiplatelet antibodies, among thrombocytopenic HIV clients at Mbarara Regional Referral Hospital, southwestern Uganda.

This was a retrospective review of hematologic results at enrollment to HIV care from 2005 to 2013. The prevalence and correlates of thrombocytopenia were estimated based on the Immune Suppressed Syndrome (ISS) Clinic electronic database. A cross-sectional study determined the occurrence of antiplatelet antibodies, using the monoclonal antibody-specific immobilization of platelet antigens (MAIPA) technique.

We reviewed 15,030 client records. The median age was 35.0 (range 18–78; interquartile range [IQR] 28–42) years, and there were 63.2% (n=9,500) females. The overall prevalence of thrombocytopenia was 17.4% (95% confidence interval [CI]: 16.8%–18.0%). The prevalence of thrombocytopenia was 17.8% (95% CI: 17.1%–18.4%) among antiretroviral therapy (ART)-naïve clients (n=2,675) and was 13.0% (95% CI: 0.3%–21.9%) for clients who were on ART (n=6). The study found a significant association between thrombocytopenia and other cytopenias, CD4 counts, ART, and deteriorating HIV stage (P<0.05). Two of the 40 participants (5.0%) had antiplatelet antibodies.

This study has showed a high prevalence of HIV-related thrombocytopenia. Antiplatelet antibodies were found in 5.0% of HIV-infected thrombocytopenic participants. Our study shows a significant association of thrombocytopenia burden in a high-HIV study population (Southwest Uganda); therefore, there is need to monitor platelet counts and initiate platelet transfusion in our blood banking practices, to avert possible risks of bleeding.

• AIDS
• antiplatelet antibodies
• cytopenia

• Autoimmunity
• HIV
• Immunosuppressant drugs

• CD16+ monocyte
• HIV
• SIV
• macaque
• platelet activation
• platelet-monocyte aggregate
• thrombocytopenia

The following state-of-the-art seminar was delivered as part of the Aspen Lung Conference on Pulmonary Hypertension and Vascular Diseases held in Aspen, Colorado in June 2012. This paper will summarize the lecture and present results from a nonhuman primate model of infection with Simian (Human) Immunodeficiency Virus - nef chimeric virions as well as the idea that polymorphisms in the HIV-1 nef gene may be driving the immune response that results in exuberant inflammation and aberrant endothelial cell (EC) function. We will present data gathered from primary HIV nef isolates where we tested the biological consequences of these polymorphisms and how their presence in human populations may predict patients at risk for developing this disease. In this article, we also discuss how a dysregulated immune system, in conjunction with a viral infection, could contribute to pulmonary arterial hypertension (PAH). Both autoimmune diseases and some viruses are associated with defects in the immune system, primarily in the function of regulatory T cells. These T-cell defects may be a common pathway in the formation of plexiform lesions. Regardless of the route by which viruses may lead to PAH, it is important to recognize their role in this rare disease.

• SHIV-nef
• endogenous retroviruses
• herpes virus
• human immunodeficiency virus
• inflammation
• nef
• pulmonary vasculopathy

Anaemia and thrombocytopenia are haematological disorders that can be detected in many human immunodeficiency virus (HIV)-positive patients during the development of HIV infection. The progressive decline of erythrocytes and platelets plays an important role both in HIV disease progression and in the clinical and therapeutic management of HIV-positive patients. HIV-dependent impairment of the megakaryocyte and erythrocyte lineages is multifactorial and particularly affects survival, proliferation and differentiation of bone marrow (BM) CD34+ haematopoietic progenitor cells, the activity of BM stromal cells and the regulation of cytokine networks. In this review, we analyse the major HIV-related mechanisms that are involved in the genesis and development of the anaemia and thrombocytopenia observed in HIV positive patients.

• Human immunodeficiency virus
• Erythrocytes
• Megakaryocytes
• Haematopoietic progenitor cells
• Virology