Association of human leukocyte antigen DQ1 and dengue fever in a white Southern Brazilian population

Memórias do Instituto Oswaldo Cruz

José Roberto Polizel¹  Danilo Bueno¹  Jeane Eliete L Visentainer¹  Ana Maria Sell¹  Sueli Donizete Borelli¹  Luiza Tamie Tsuneto¹  Marcia Machado O Dalalio¹  Maria Teresa M Coimbra¹  Ricardo Alberto Moliterno¹ 

[1] ,Universidade Estadual de Maringá Departamento de Análises Clínicas Maringá PR ,Brasil

关键词: human leukocyte antigens;    dengue fever;    Brazil;   

DOI  :  10.1590/S0074-02762004000600003

来源: SciELO

【 摘 要 】

Dengue is an infectious disease of viral etiology transmitted by the mosquitoes Aedes aegypti, A. albopictus, and A. scutellaris. It can develop either as a benign form or as a severe hemorrhagic form. Previous work showed an association of the hemorrhagic form with human leukocyte antigens (HLA), suggesting a role of genetic factors in disease susceptibility. Nevertheless, data on HLA association with the classical form of the disease is scarce in literature. Sixty-four patients and 667 normal individuals, living in the state of Paraná, Southern Brazil, were used as test and control group, respectively. The patients developed the disease during a virus 1 dengue outbreak either in Maringá city in 1995 (47) or in Paranavaí city in 1999 (17). The diagnostic was confirmed through serology and/or viral culture. HLA class I and II typing was performed by the classical microlynfocitotoxicity test using monoclonal antisera and fluorobeads. Qui-square statistical analysis confirmed a positive association with HLA-DQ1 (76.6% vs 57.7%; p = 0.005243; pc = 0.026215). HLA-DR1 also presented an increased frequency in the test group, not statistically significant after p correction though (32.8% vs 15.9%; p = 0.005729; pc = 0.080206). In conclusion, genetic factors may play a role on the susceptibility to the classical dengue, virus 1, in the Brazilian population. Further independent studies should be performed in the Brazilian population to confirm these preliminary data.

【 授权许可】

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