Published online Jun 18, 2015. doi: 10.4254/wjh.v7.i11.1572
Peer-review started: September 20, 2014
First decision: December 17, 2014
Revised: January 30, 2015
Accepted: March 30, 2015
Article in press: April 2, 2015
Published online: June 18, 2015
Processing time: 271 Days and 14.7 Hours
Hepatocellular carcinoma (HCC), the predominant type of primary liver cancer, is one of the most serious life-threatening malignancies, worldwide. In majority of the cases, HCC develops after prolonged and persistent chronic liver disease. hepatitis B virus (HBV) or HCV infection is prominent etiological factors, attributing to this condition. It has been well documented that HBV, being the inducer of chronic inflammation, is the main causative agent in causing HCC, particularly in Asian countries. The HBV infection leads to a wide range of clinical symptoms from carrier state to malignancy. Cytokines being immune-modulatory molecules, are the key mediators in the defense mechanism against viral infection. In this regard, this review will detail the substantial role of key Th1: interleukin 1 (IL-1), IL-2, IL-12, tumor necrosis factor-α, interferon-γ; Th2: IL-4, IL-10 and non Th1/Th2: IL-6, transforming growth factor-β1 cytokines genotypes in analyzing the variability in the clinical manifestations in an HBV-afflicted individual, which might finally, culminates into HCC. Since cytokine production is regulated genetically, the cytokine promoter region single-nucleotide polymorphisms induced changes, greatly affects the cytokine production, thus resulting into differential outcome of immune balance.
Core tip: Hepatocellular carcinoma is the prime manifestation of primary liver cancer. Besides, hepatitis B virus (HBV) infection accounts for nearly 50% of hepatocellular carcinoma cases worldwide. The injuries afflicted by HBV infection are predominantly immune-mediated. Th1/Th2 cytokines play a significant role in modulating almost all phases of the host immune response. Moreover, cytokine production and response is genetically controlled. Hence, the population-based variability in patterns of cytokine polymorphisms, might alter the ability of an individual to mount an appropriate immune response, thus causing a differential effect on the progression of the HBV disease pathogenesis.