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BioMed Research International
Volume 2017 (2017), Article ID 1728456, 12 pages
Research Article

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

1Instituto de Investigaciones Biomédicas en Retrovirus y Sida (INBIRS), Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Piso 11, C1121ABG Buenos Aires, Argentina
2Laboratorio de Virología y Genética Molecular (LVGM), Facultad de Ciencias Naturales y Ciencias de la Salud Sede Trelew, Universidad Nacional de la Patagonia San Juan Bosco, 9 de Julio y Belgrano S/N, Chubut, 9100 Trelew, Argentina
3Consejo Nacional de Investigaciones Científicas y Técnicas, Av. Rivadavia 1917, C1083ACA Buenos Aires, Argentina

Correspondence should be addressed to Jorge Quarleri; ra.abu.demf@irelrauq

Received 8 August 2017; Accepted 19 October 2017; Published 12 November 2017

Academic Editor: Fumio Imazeki

Copyright © 2017 Micaela Parra et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.