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

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Název: Phylogenetic Diversity in Core Region of Hepatitis C Virus Genotype 1a as a Factor Associated with Fibrosis Severity in HIV-1-Coinfected Patients
Autoři: Micaela Parra, Natalia Laufer, Julieta M. Manrique, Leandro R. Jones, Jorge Quarleri
Zdroj: Biomed Res Int
CONICET Digital (CONICET)
Consejo Nacional de Investigaciones Científicas y Técnicas
Informace o vydavateli: Wiley, 2017.
Rok vydání: 2017
Témata: Liver Cirrhosis, Male, 0301 basic medicine, Genotype, Liver fibrosis, HIV Infections, Hepacivirus, phylogeny, 03 medical and health sciences, Risk Factors, Humans, Phylogeny, 0303 health sciences, Coinfection, core, HIV, Genetic Variation, Interferon-alpha, Hepatitis C, Chronic, genotype 1a, 3. Good health, HCV, HIV-1, Female, Research Article
Popis: 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.
Druh dokumentu: Article
Other literature type
Popis souboru: text/xhtml; application/pdf
Jazyk: English
ISSN: 2314-6141
2314-6133
DOI: 10.1155/2017/1728456
Přístupová URL adresa: http://downloads.hindawi.com/journals/bmri/2017/1728456.pdf
https://pubmed.ncbi.nlm.nih.gov/29259976
https://www.ncbi.nlm.nih.gov/pubmed/29259976
https://core.ac.uk/display/132174632
https://doi.org/10.1155/2017/1728456
https://www.hindawi.com/journals/bmri/2017/1728456/
https://ri.conicet.gov.ar/handle/11336/47446
http://downloads.hindawi.com/journals/bmri/2017/1728456.pdf
http://hdl.handle.net/11336/47446
Rights: CC BY
CC BY NC SA
Přístupové číslo: edsair.doi.dedup.....62116b3f44989b1b2422e57c1fb43344
Databáze: OpenAIRE
Popis
Abstrakt: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.
ISSN:23146141
23146133
DOI:10.1155/2017/1728456