Relating the outcome of HCV infection and different host SNP polymorphisms in a Majorcan population coinfected with HCV–HIV and treated with pegIFN-RBV

Authors

  • Marina Matas University Institute of Research in Health Sciences and Laboratory of Genetics, Department of Biology, University of the Balearic Islands, Palma, Spain.
  • Antònia Picornell University Institute of Research in Health Sciences and Laboratory of Genetics, Department of Biology, University of the Balearic Islands, Palma, Spain.
  • Carmen Cifuentes Infectious Diseases Center, Son Llàtzer Hospital, Palma.
  • Antoni Payeras Infectious Diseases Center, Son Llàtzer Hospital, Palma.
  • Francesc Homar Infectious Diseases Center, Son Llàtzer Hospital, Palma.
  • Fernando González-Candelas Joint Unit Genomics and Health, FISABIO-Public Health Research/Cavanilles Institute of Biodiversity and Evolutionary Biology, University of València, València, CIBER in Epidemiology and Public Health, Carlos III Health Institute, Spain
  • F. Xavier López-Labrador Joint Unit Genomics and Health, FISABIO-Public Health Research/Cavanilles Institute of Biodiversity and Evolutionary Biology, University of València, València, CIBER in Epidemiology and Public Health, Carlos III Health Institute, Spain
  • Andrés Moya Joint Unit Genomics and Health, FISABIO-Public Health Research/Cavanilles Institute of Biodiversity and Evolutionary Biology, University of València, València, CIBER in Epidemiology and Public Health, Carlos III Health Institute, Spain
  • Cori Ramon University Institute of Research in Health Sciences and Laboratory of Genetics, Department of Biology, University of the Balearic Islands, Palma.
  • José A. Castro University Institute of Research in Health Sciences and Laboratory of Genetics, Department of Biology, University of the Balearic Islands, Palma, Spain.

Keywords:

HCV–HIV co-infection, mtDNA haplogroups, SNP polymorphisms

Abstract

Hepatitis C virus (HCV) is one of the major causes of chronic hepatitis, cirrhosis, and hepatocellular carcinoma, and the development of HCV-related disease is accelerated in individuals coinfected with human immunodeficiency-1 virus (HIV). In the present study, we correlated different host single-nucleotide polymorphisms (SNPs) in the IL28B, CTLA4, LDLr, and HFE genes and mitochondrial DNA (mtDNA) haplogroups with the outcome of HCV infection and the response to pegylated-interferon plus ribavirin (pegIFN-RBV) treatment. Our study population consisted of 63 Majorcan patients coinfected with HCV and HIV and 59 anonymous unrelated controls. Whereas the population frequency of IL28B alleles was similar to that found in a North-American cohort of European descent, the frequency of the rs12979860 C allele was lower than that determined in other cohorts from Spain. The frequencies of CTLA4 and LDLr polymorphisms were comparable to those reported in other populations. Significant differences between cases and control cohorts occurred only for the H63D mutation of the HFE gene. There were no other differences in the frequencies of other polymorphisms or mtDNA haplogroups. The IL28B rs12979860 CC genotype was shown to be associated with a rapid virological response, and the spontaneous viral clearance rate for HCV was higher in patients with the CTLA4+49 G allele. There was no relationship between SNPs in the LDLr and HFE genes and mtDNA haplogroups and the response to treatment. Our results suggest that the host genetic background plays a significant role in the pegIFN-RBV response of patients coinfected with HCV and HIV. [Int Microbiol 2014; 17(1):11-20]

Keywords: HCV–HIV co-infection · mtDNA haplogroups · SNP polymorphisms

Downloads

Issue

Vol. 17 No. 1 (2014)

Section

Research Articles

License

Submission of a manuscript to International Microbiology implies: that the work described has not been published before, including publication in the World Wide Web (except in the form of an Abstract or as part of a published lecture, review, or thesis); that it is not under consideration for publication elsewhere; that all the coauthors have agreed to its publication. The corresponding author signs for and accepts responsability for releasing this material and will act on behalf of any and all coauthors regarding the editorial review and publication process.

If an article is accepted for publication in International Microbiology, the authors (or other copyright holder) must transfer to the journal the right–not exclusive–to reproduce and distribute the article including reprints, translations, photographic reproductions, microform, electronic form (offline, online) or any other reproductions of similar nature. Nevertheless, all article in International Microbiology will be available on the Internet to any reader at no cost. The journal allows users to freely download, copy, print, distribute, search, and link to the full text of any article, provided the authorship and source of the published article is cited. The copyright owner's consent does not include copying for new works, or resale. In these cases, the specific written permission of International Microbiology must first be obtained.

Authors are requested to create a link to the published article on the journal's website. The link must be accompanied by the following text: "The original publication is available on LINK at <http://www.im.microbios.org>. Please use the appropiate URL for the article in LINK. Articles disseminated via LINK are indexed, abstracted, and referenced by many abstracting and information services, bibliographic networks, subscription agencies, library networks, and consortia.