CD81 expression in peripheral blood lymphocytes before and after treatment with interferon and ribavirin in HIV/HCV coinfected patients.

Background CD81 is expressed on lymphocytes and confers HCV viral infectivity support. The aim of our study was to quantify CD81 expression in peripheral blood B- and T-cells of HCV/HIV-coinfected patients and healthy subjects to examine its association with several HCV virological characteristics and the therapeutic responsiveness to HCV antiviral treatment. Methods We carried out a cross-sectional study on 122 naive patients. For a duration of 48 weeks, 24 out of 122 patients underwent HCV antiviral therapy with interferon (IFN)-alpha and ribavirin. T- and B-cell subsets were analysed by flow cytometry. Results We found that HIV/HCV coinfected patients with HCV-RNA >= 850 000 IU/mL had lower values of %CD19 + CD81-CD62L + and %CD19 + CD62L + ; and higher values of CD19 + CD81 + CD62L - and CD19 + CD81 + percentages and absolute counts than patients with HCV-RNA < 850 000 IU/mL. Similarly, HIV/HCV coinfected patients with the genotype 1 had lower values of %CD19 + CD81 - CD62L + and higher values of CD3 + CD81 + CD62L - and CD3 + CD81 + percentages and absolute counts than patients without genotype 1. Moreover, we found that HIV/HCV coinfected patients had higher values of %CD19 + HLA-DR + CD25 + , %CD19 + CD40 + CD25 + and %CD19 + CD25 + than healthy control patients. When we studied the B- and T-cell subset kinetics of 24 HIV/HCV coinfected patients on HCV antiviral therapy, we found a significant decrease in CD3 + CD81 + and CD3 + CD81 + CD62L - subsets and a significant increase in CD3 + CD62L + and CD3 + CD81 + CD62L + percentages and absolute counts, but the variation in these markers disappeared several months after stopping the treatment. Conclusions We observed a different pattern of CD81 T-cell and B-cell levels in naive HIV/HCV coinfected patients according to HCV virological status and their subsequent variations during HCV antiviral treatment. CD81 expression might influence HCV pathogenesis and response to HCV antiviral treatment.