title: Upregulation of soluble and membrane-bound human leukocyte antigen G expression is primarily observed in the milder histopathological stages of chronic hepatitis C virus infection.
abstract: Chronic hepatitis C virus (HCV) infection is a worldwide health problem that may evolve to cirrhosis and hepatocellular carcinoma. Incompletely understood immune system mechanisms have been associated with impaired viral clearance. The nonclassical class I human leukocyte antigen G (HLA-G) molecule may downregulate immune system cell functions exhibiting well-recognized tolerogenic properties. HCV genotype was analyzed in chronic HCV-infected patients. Because HLA-G expression may be induced by certain viruses, we evaluated the presence of HLA-G in the liver microenvironment obtained from 89 biopsies of patients harboring chronic HCV infection and stratified according to clinical and histopathological features. Overall, data indicated that HCV genotype 1 was predominant, especially subgenotype 1a, with a prevalence of 87%. HLA-G expression was observed in 45 (51%) liver specimens, and it was more frequent in milder stages of chronic hepatitis (67.4%) than in moderate (27.8%; p = 0.009) and severe (36.0%; p = 0.021) stages of the disease. Altogether, these results suggest that the expression of HLA-G in the context of HCV is a complex process modulated by many factors, which may contribute to an immunologic environment favoring viral persistence. However, because the milder forms predominantly expressed HLA-G, a protective role of this molecule may not be excluded.
authors.affiliation: Department of Clinical Analysis and Toxicology, Federal University of Rio Grande do Norte, Natal, CEP 59012-570, Brazil. janacrispim@hotmail.com
authors.forename: Janaina Cristiana
authors.initials: JC
authors.lastname: de Oliveira Crispim
authors.forename: Tarsia Giabardo Alves
authors.initials: TG
authors.lastname: Silva
authors.forename: Francisco José Dutra
authors.initials: FJ
authors.lastname: Souto
authors.forename: Fernanda Fernandes
authors.initials: FF
authors.lastname: Souza
authors.forename: Carmen Lucia
authors.initials: CL
authors.lastname: Bassi
authors.forename: Christiane Pienna
authors.initials: CP
authors.lastname: Soares
authors.forename: Sérgio
authors.initials: S
authors.lastname: Zucoloto
authors.forename: Philippe
authors.initials: P
authors.lastname: Moreau
authors.forename: Ana de Lourdes Candolo
authors.initials: Ade L
authors.lastname: Martinelli
authors.forename: Eduardo Antonio
authors.initials: EA
authors.lastname: Donadi
mesh_terms: D000328:Adult; D000368:Aged; D004279:DNA, Viral / Q000032:analysis; D018450:Disease Progression; D005260:Female; D005838:Genotype; D059951:HLA-G Antigens / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity; D019698:Hepatitis C, Chronic / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology / Q000821:virology; D006801:Humans; D057131:Immune Evasion; D007150:Immunohistochemistry; D008099:Liver / Q000276:immunology / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D008297:Male; D008875:Middle Aged; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D004279:DNA, Viral; D059951:HLA-G Antigens