ABSTRACT
Severe forms of dengue, such as dengue haemorrhagic fever (DHF) and dengue shock syndrome, are examples of a complex pathogenic mechanism in which the virus, environment and host immune response interact. The influence of the host's genetic predisposition to susceptibility or resistance to infectious diseases has been evidenced in several studies. The association of the human leukocyte antigen gene (HLA) class I alleles with DHF susceptibility or resistance has been reported in ethnically and geographically distinct populations. Due to these ethnic and viral strain differences, associations occur in each population, independently with a specific allele, which most likely explains the associations of several alleles with DHF. As the potential role of HLA alleles in the progression of DHF in Brazilian patients remains unknown, we then identified HLA-A alleles in 67 patients with dengue fever and 42 with DHF from Rio de Janeiro, Brazil, selected from 2002-2008 by the sequence-based typing technique. Statistical analysis revealed an association between the HLA-A*01 allele and DHF [odds ratio (OR) = 2.7, p = 0.01], while analysis of the HLA-A*31 allele (OR = 0.5, p = 0.11) suggested a potential protective role in DHF that should be further investigated. This study provides evidence that HLA class I alleles might be important risk factors for DHF in Brazilian patients.
Subject(s)
Adolescent , Adult , Aged , Aged, 80 and over , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Young Adult , Severe Dengue/genetics , Genetic Predisposition to Disease/genetics , HLA-A1 Antigen/genetics , Alleles , Brazil , Case-Control Studies , Risk FactorsABSTRACT
Dengue infection is a major public health problem. The mechanisms underlying severe bleeding in dengue DHF are not completely understood. It was proposed that the dengue virus nonstructural- 1 protein [DNS 1] generated antibodies to common epitopes on human blood clotting and integrinladhesin proteins on the platelet. The proof on the functional correlation between DNS 1 and platelet integrinladhesin proteins is needed. Here, the author used a new gene ontology technology to predict th molecular function and biological process of DNS 1 and platelet integrinladhesin proteir, CD6 1. According to this study, the author can identify no function and biological process of DNS1. Also, there is no existence of functional similarity between DNS1 and CD61. The hypothesis on role of molecular mimicry between DNS1 and CD61 is not supported in this study