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Modulation of HCV replication after combination antiretroviral therapy in HCV/HIV co-infected patients

Treatment of HIV patients co-infected with hepatitis C virus (HCV) with HIV antiretroviral drug therapy reduces HCV replication. Treating One Virus to Suppress Another There is a complex interaction of biological effects when patients are infected with both HIV and the hepatitis C virus (HCV). In a new study of patients co-infected with HCV and HIV, Sherman et al. try and unravel some of these biological effects. They show that the initial response to effective HIV treatment results in a transient increase in HCV viral replication and evidence of liver injury. Over time, however, HIV suppression leads to reduced HCV replication. This process is highly modulated by responses of the interferon-responsive gene family. The findings suggest that HIV suppression with antiretroviral medications plays an important role in the management of those with HCV and HIV infection. The hepatitis C virus (HCV) is an important contributor to morbidity and mortality in patients co-infected with HIV. Co-infection results in increased HCV replication and more rapid rates of liver disease progression. The effect of HIV combination antiretroviral therapy (cART) on HCV replication has not been studied in depth. To address this issue, we enrolled a small cohort of HCV/HIV co-infected patients into a cART initiation trial and used dynamic modeling combined with evaluation of immune responses and microarray profiles to determine how effective treatment of HIV affects HCV. Treatment with cART resulted in increased HCV replication and increased alanine aminotransferase (ALT) in a subset of patients. Subjects with evidence of hepatic injury (increased ALT) were more likely to have HCV-specific immune responses directed against HCV epitopes. Over time, HCV viral loads declined. Reproducible and biologically important gene expression changes occurred in co-infected patients who underwent successful cART. The effective suppression of HIV by cART initiated a cascade of early and late events in treated patients. Early events involving down-regulation of interferon-stimulated genes may have led to transiently increased viral replication and hepatic injury. At later time points, HCV viral load declined to levels comparable to those seen in the setting of HCV monoinfection. These findings support early antiretroviral therapy in those with HCV/HIV co-infection.