Evolution of hepatitis C virus in HIV coinfected patients under antiretroviral therapy

Sede, Mariano Miguel; Parra, Micaela; Manrique, Julieta M.; Laufer, Natalia; Jones, Leandro Roberto; Quarleri, Jorge

doi:10.1016/j.meegid.2016.05.032

Cited by 1 publication

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“…All haplotypes characterized were patient-specific, meaning that there were no haplotypes shared between different individuals for the entire follow-up ( Figure 2 ). In addition, each patient's haplotypes were highly related to each other compared to the haplotypes from other patients ( Figure 2 ), in agreement with previous studies [ 36 , 37 ]. The only exceptions were patients H and X (and in a lesser extent patient S), whose sequences were sparse across the phylogeny in the case of patient H and grouped in two different clades for patient X ( Figure 2 ).…”

Section: Resultssupporting

confidence: 91%

Phylogenetic Diversity in Core Region of Hepatitis C Virus Genotype 1a as a Factor Associated with Fibrosis Severity in HIV-1-Coinfected Patients

Parra

Laufer

Manrique

et al. 2017

BioMed Research International

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High hepatitis C virus (HCV) genetic diversity impacts infectivity/pathogenicity, influencing chronic liver disease progression associated with fibrosis degrees and hepatocellular carcinoma. HCV core protein is crucial in cell-growth regulation and host-gene expression. Liver fibrosis is accelerated by unknown mechanisms in human immunodeficiency virus-1- (HIV-1-) coinfected individuals. We aimed to study whether well-defined HCV-1a core polymorphisms and genetic heterogeneity are related to fibrosis in a highly homogeneous group of interferon-treated HIV-HCV-coinfected patients. Genetic heterogeneity was weighed by Faith's phylogenetic diversity (PD), which has been little studied in HCV. Eighteen HCV/HIV-coinfected patients presenting different liver fibrosis stages before anti-HCV treatment-initiation were recruited. Sampling at baseline and during and after treatment was performed up to 72 weeks. At inter/intrahost level, HCV-1a populations were studied using molecular cloning and Sanger sequencing. Over 400 complete HCV-1a core sequences encompassing 573 positions of C were obtained. Amino acid substitutions found previously at positions 70 and 91 of HCV-1b core region were not observed. However, HCV genetic heterogeneity was higher in mild than in severe fibrosis cases. These results suggest a potential utility of PD as a virus-related factor associated with chronic hepatitis C progression. These observations should be reassessed in larger cohorts to corroborate our findings and assess other potential covariates.

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Section: Resultssupporting

confidence: 91%