HCV RNA viral load is independent from CD4 cell count and plasma HIV RNA viral load in immunocompetent HIV-HCV co-infected patients: a 3-years follow-up study

Abstract

Background: HCV 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).

Methods: We 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.

Results: HCV 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.

Conclusions: The 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.

Keywords: Follow-up; HCV RNA; HCV genotype 1; HIV RNA; Interleukin 28B CC allele.

Figure 1

Flow chart describing the selection of the study patients.

Figure 2

Antiretroviral drug regimens of the 73 co-infected patients treated in 2012 (data available for 70/73 patients, 95.6%): for each drug combination are reported both percentage respect to the number of treated patients and absolute number. Legend: ABC = abacavir; AZT = zidovudine; FTC = emtricitabine; MVC = maraviroc; NNRTI = non-nucleoside reverse transcriptase inhibitors; PI = protease inhibitor; RLT = raltegravir; TDF = tenofovir; 3TC = lamivudine.

Figure 3

Study design overview. Initial Follow-Up (IFU) started at T1 (in 2009) and lasted 2 years, Final Follow-Up (FFU) started at the end of IFU, lasted one year and finished at T2, in 2012.