title: Polymorphisms in human leukocyte antigens, human platelet antigens, and cytokine genes in hantavirus cardiopulmonary syndrome patients from Ribeirão Preto, Brazil.
abstract: Hantavirus cardiopulmonary syndrome is a severe human disease associated with hantavirus infection. The clinical course of illness varies greatly among individuals, possibly due to viral and immunological elements and the influence of host genetic factors on clinical outcome. As the magnitude of immune activation has been associated with disease severity, polymorphisms in genes involved in the immune response that may affect the development of this syndrome were investigated. Polymorphisms in the TGF-β, IL-10, IL-6, and IFN-γ genes, human leukocyte antigens (HLA), and human platelet alloantigens (HPA) genes were investigated in 122 patients with Araraquara virus infection from Ribeirão Preto, Brazil. Patients were divided into two groups: hantavirus cardiopulmonary syndrome (HCPS group; n = 26) and hantavirus seropositive only (n = 96). The frequencies of HLA alleles, cytokines and platelet antigen genotypes were evaluated in both groups and compared to a control group. The data demonstrated no significant influence of the HLA alleles, HPA, IL-6, and IL-10 genotypes on susceptibility to hantavirus infection. However, the hantavirus seropositive group presented a significantly higher frequency of a polymorphism associated with a high IFN-γ production than the HCPS group. In addition, a genotype associated with high TGF-β production was found more frequently in individuals infected with hantavirus than in the control group. This phenotype was associated with a less intense thrombocytopenia in the HCPS group and may be protective against the most severe form of hantavirus disease. More studies are required to quantify further the influence of the high TGF-β producer phenotype on the outcome of hantavirus infection.
authors.affiliation: Virology Research Center, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
authors.forename: Alessandra Abel
authors.initials: AA
authors.lastname: Borges
authors.forename: Eduardo Antonio
authors.initials: EA
authors.lastname: Donadi
authors.forename: Gelse Mazzoni
authors.initials: GM
authors.lastname: Campos
authors.forename: Glauciane Garcia
authors.initials: GG
authors.lastname: de Figueiredo
authors.forename: Fabiano Pinto
authors.initials: FP
authors.lastname: Saggioro
authors.forename: Soraya Jabur
authors.initials: SJ
authors.lastname: Badra
authors.forename: Neifi Hassan Saloum
authors.initials: NH
authors.lastname: Deghaide
authors.forename: Luiz Tadeu Moraes
authors.initials: LT
authors.lastname: Figueiredo
mesh_terms: D000293:Adolescent; D000328:Adult; D016824:Antigens, Human Platelet / Q000235:genetics*; D001938:Brazil; D016207:Cytokines / Q000235:genetics*; D004198:Disease Susceptibility; D005260:Female; D006680:HLA Antigens / Q000235:genetics*; D018804:Hantavirus Pulmonary Syndrome / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D055815:Young Adult
chemical_list: D016824:Antigens, Human Platelet; D016207:Cytokines; D006680:HLA Antigens
keywords: HLA; TGF-β; cardiopulmonary syndrome; genetic polymorphisms; hantavirus