title: HLA-G regulatory polymorphisms are associated with susceptibility to HCV infection.
abstract: Hepatitis C virus (HCV) is able to bypass the immune system modulating innate and adaptive immune response and blocking T helper 1 (Th1) cell production. Because the human leukocyte antigen (HLA)-G molecule has immunomodulatory properties inhibiting the function and production of natural killer and cytotoxic lymphocyte T cells, as well as promoting shift from Th1 toward Th2 response, we hypothesized its involvement in susceptibility to HCV infection.
  
  
  
  Considering that HLA-G mRNA expression has been reported to be under genetic control, an association study was conducted analyzing 800 base pairs upstream the ATG at the 5'upstream regulator region (URR) and 850 base pairs from ATG to exon 3 and the 3'untranslated region (UTR) of HLA-G gene in Italian HCV-positive patients and uninfected controls.
  
  
  
  Four 5'URR polymorphisms (-725C>G>T, -509C>G, -400G>A and -398G>A), 7 polymorphisms at coding region (+15G>A, +36G>A, +243G>A, insC506, 531G>C, delA615 and 685G>A), the +644G>T polymorphism, and 1 haplotype (TTGTTCCIGAC) showed different frequency distributions between HCV patients and uninfected controls.
  
  
  
  The results from our study suggest a possible involvement of HLA-G in the risk modulation toward HCV infection.
authors.affiliation: Department of Medicine, Surgery and Health Sciences, University of Trieste, Trieste, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Catamo
authors.affiliation: Institute for Maternal and Child Health, IRCCS "Burlo Garofolo", Trieste, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Zupin
authors.affiliation: Department of Life Science, University of Trieste, Trieste, Italy.
authors.forename: N
authors.initials: N
authors.lastname: Freato
authors.affiliation: Institute for Maternal and Child Health, IRCCS "Burlo Garofolo", Trieste, Italy.
authors.forename: V
authors.initials: V
authors.lastname: Polesello
authors.affiliation: Institute for Maternal and Child Health, IRCCS "Burlo Garofolo", Trieste, Italy.
authors.forename: F
authors.identifier: 0000-0002-9760-8463
authors.initials: F
authors.lastname: Celsi
authors.affiliation: Department of Medicine, Surgery and Health Sciences, University of Trieste, Trieste, Italy.
authors.forename: S L
authors.initials: SL
authors.lastname: Crocè
authors.affiliation: Department of Medicine, Surgery and Health Sciences, University of Trieste, Trieste, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Masutti
authors.affiliation: Department of Medicine, Surgery and Health Sciences, University of Trieste, Trieste, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Pozzato
authors.affiliation: Institute for Maternal and Child Health, IRCCS "Burlo Garofolo", Trieste, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Segat
authors.affiliation: Department of Medicine, Surgery and Health Sciences, University of Trieste, Trieste, Italy.|Institute for Maternal and Child Health, IRCCS "Burlo Garofolo", Trieste, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Crovella
mesh_terms: D020413:3' Untranslated Regions; D020121:5' Untranslated Regions; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D016022:Case-Control Studies; D005091:Exons; D005260:Female; D015870:Gene Expression; D005787:Gene Frequency; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D059951:HLA-G Antigens / Q000235:genetics* / Q000276:immunology; D006239:Haplotypes; D016174:Hepacivirus / Q000276:immunology*; D006526:Hepatitis C / Q000175:diagnosis / Q000235:genetics* / Q000276:immunology / Q000821:virology; D006801:Humans; D007558:Italy; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D012306:Risk; D018417:Th1 Cells / Q000276:immunology / Q000821:virology
chemical_list: D020413:3' Untranslated Regions; D020121:5' Untranslated Regions; D059951:HLA-G Antigens
keywords: hepatitis C virus; human leukocyte antigen-G; immunity; single nucleotide polymorphism