Abstract

BackgroundHCV RNA viral load is an important predictor of sustained virological response and, recently, a significant correlation with liver fibrosis was described. We investigated on possible influence of clinical and viro-immunological variables on HCV viral load in HIV-HCV co-infected patients over a study time of three years (2009-2012).MethodsWe retrospectively enrolled 98 adult patients with a diagnosis of chronic HIV infection in 2009, a diagnosis of chronic HCV infection with a detectable plasma HCV RNA in 2009 and 2012, HCV therapy-naïve or with failed and stopped antiviral treatment before June 2008. The following variables were recorded: age, gender, HCV genotype, IL28B rs12979860 CC genotype, HCV treatment status, advanced liver fibrosis diagnosis, antiretroviral therapy, CD4+ cell count, HCV viral load, HIV RNA (plasma HIV-1 RNA levels were measured from blood samples every three months at least). The correlation was established using linear regression analysis, analysis of variance and Fisher’s exact test. Comparisons between groups were performed using Fisher’s exact test, the independent samples t-test and the t-test for paired data, as appropriate, for continuous variables. A mixed mode (ME) maximum likelihood linear regression model was constructed to evaluate the dependence of HCV viral load.ResultsHCV RNA levels did not change significantly from 2009 to 2012 (from 3924650 ± 5320177 IU/ml to 3085128 ± 3372347 IU/ml, p = 0.13); the CD4+ count increased significantly (from a mean of 576 to a mean of 654, p = 0.003). Using linear regression, a positive correlation was observed for HCV load and genotype 1 (p = 0.002), nonresponder status (p = 0.04) and with interleukin 28B CC allele (p = 0.05). Other studied covariates failed to reach a significant correlation.ConclusionsThe HCV RNA load, a known pretreatment predictor of response to antiviral therapy, was independent of the two main parameters of HIV disease, plasma HIV RNA and CD4 cell count, over an observation time of 3 years in patients with recovered or spontaneously maintained immunocompetence.

Highlights

  • Hepatitis C virus (HCV) RNA viral load is an important predictor of sustained virological response and, recently, a significant correlation with liver fibrosis was described

  • The timing of human immunodeficiency virus (HIV) and HCV therapies must be individualized and tailored based on personal patient clinical characteristics, which can change with time; this approach is especially recommended for HIV patients with HCV genotype 1 infection, who may be candidates for antiviral treatment, including direct-acting antiviral drugs (DAAs) [5]

  • The HCV RNA viral load is thought to play a role in fields other than antiviral treatment; Kirk et al [11] reported a significant correlation between liver fibrosis and HCV RNA load (p < 0.001) in a cohort of 1176 HCVpositive subjects (34% with HIV coinfection)

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Summary

Introduction

HCV RNA viral load is an important predictor of sustained virological response and, recently, a significant correlation with liver fibrosis was described. The recently published European AIDS Clinical Society Guidelines stated that a low pretreatment HCV RNA value is 400,000-600,000 IU/mL [7]. A pretreatment HCV RNA viral load < 600,000 IU/ml is significantly associated with SVR in co-infected patients treated with pegylated interferon and ribavirin (p < 0.001) [8], even in subjects with compensated cirrhosis (p = 0.01) [9]; a value higher than this threshold is a predicting factor for relapse (p = 0.02) in the study by Rivero-Juarez et al [10]. The HCV RNA viral load is thought to play a role in fields other than antiviral treatment; Kirk et al [11] reported a significant correlation between liver fibrosis and HCV RNA load (p < 0.001) in a cohort of 1176 HCVpositive subjects (34% with HIV coinfection)

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