Success of antiviral therapy in chronic hepatitis C infection relates to functional status of myeloid dendritic cells.

Chronic hepatitis C infection poses a major global health predicament and appears to be potent threat to mankind. The treatment in wide use is interferon/ribavirin combination therapy which is generally effective in about 60-70 per cent of patients carrying genotype 3 and causes significant morbidity. The response to therapy is largely guided by limited number of factors such as genotype of virus, rapid virological response, ethnicity, pre-therapy viral load, etc. While involvement of host genetic factors has been a major focus of research in playing an important role in the outcome of disease, the role of immune system cannot be marginalized. Poor cellular trafficking and suboptimal T cell responses in liver, the hall marks of chronic hepatitis C virus infection, might be attributed to defective antigen presentation. Various immunological factors, both innate and adaptive, play role in the pathogenesis of the disease and become dysfunctional in active disease. Recent reports suggest the major impact of functional and numerical status of dendritic cells in deciding the fate of antiviral therapy. In this review we take a look at the involvement of dendritic cells in playing an important role in the response to therapy.

HBV specific T-cell responses in hepatitis B.

Background: Cellular immune responses seem to prevail in acute hepatitis, whereas chronically infected patients demonstrate generally suppressed cellular immune responses and significantly greater antibody responses. Aim: To study hepatitis B virus (HBV) specific T cell proliferative responses in HBV related liver diseases. Methods: We analyzed the T lymphocyte proliferative responses to the nonspecific mitogen phytohemagglutinin (PHA) and the HBV specific hepatitis B core antigen (HBcAg) by calculating T cell proliferation index in 10 acute viral hepatitis (AVH) patients, 19 chronic hepatitis B (CHB) patients, 10 HBV cirrhotics, 10 inactive carriers and 10 healthy controls using MTT assay. Results: The mean proliferation index (PI) to PHA was highest in healthy controls (133.2 + 58.1) and lowest in cirrhotics (44.1 + 46.9) with all other groups falling in between. On comparing the mean T cell responses to HBcAg, AVH patients had the highest mean response (186.48 + 116.37) followed by CHB (137.9 + 134.3), inactive carriers (63.2 + 41.2) and cirrhotics (55.5 + 42.7). Conclusions: Patients with AVH had the highest T cell response to HBcAg, which probably explains the clearance of virus in these patients, in contrast to patients with cirrhosis who had the lowest T cell response.