Monocyte activation by interferon-α is associated with failure to achieve a sustained virologic response after treatment for hepatitis C virus infection. Interferon-alpha (IFN-α) and ribavirin can induce a sustained virologic response (SVR) in some but not all hepatitis C virus (HCV)-infected patients. The mechanism of effective treatment is unclear. One possibility is that IFN-α differentially improves the functional capacity of classic myeloid dendritic cells (mDC) by altering expression of surface molecules or cytokines. Others have proposed that antigen-presenting cell activation could be paradoxically detrimental in HCV due to the production by monocytes of substances inhibitory or toxic to plasmacytoid dendritic cells. We examined responses to in vitro IFN-α treatment of peripheral blood leukocyte samples from a retrospective treatment cohort of nearly 200 HCV-seropositive patients who had undergone antiviral therapy with ribavirin and peginterferon. We analyzed the variable responses of antigen-presenting cell subsets to drug.
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