Abstract
Human leukocyte antigen (HLA) class I molecules of the human major histocompatibility complex (MHC) play an important role in modulating immune response. HLA class I molecules present antigenic peptides to CD8+ T cells and thereby play a role in the immune surveillance of cells infected with viruses. TAP1 and TAP2 are MHC-II-encoded genes necessary for the generation of a cellular immune response and polymorphism of these genes can influence the specificity of peptides preferentially presented by the MHC class I molecules and the outcome of the immune response. Several studies implicated genetic variation in TAP genes to various immune-mediated and infectious diseases. To determine the correlation between HIV-1 infection and the TAP1 and TAP2 genes polymorphisms, we performed PCR–RFLP assay of these genes in 500 HIV-1 seropositives and the matched seronegative individuals. Statistical analysis of the data disclosed no correlation between TAP1 (C/T intron 7) gene polymorphism and HIV-1/AIDS disease. However, the current results demonstrated that the heterozygous A/G [OR (95% CI) 1.39 (1.06–1.83), P = 0.0171] and homozygous G/G [OR (95% CI) 3.38(1.56–7.46), P = 0.0010] variants of TAP2 (A/G exon 11) (T665A) gene are positively associated with an increased risk of HIV-1/AIDS infection. This case–control analysis might suggest a possible role of TAP2 (A/G exon 11) (T665A) gene in the susceptibility to HIV-1 infection and disease outcome among North Indian patients.
Highlights
The human immunodeficiency virus infection (HIV) is essentially an infection of the immune system, with progressive and profound defects in the cell-mediated immune response, in which viral and host genetic factors may have an important role [1, 2]
HIV infection results in a progressive loss of the CD4+ T helper cells, leading to severe immunosuppression that predisposes a patient to wide range of opportunistic infections, malignant neoplasm, and neurological complications that rarely occur in persons with intact immune function [31, 32]
Genetic variations in human population exert a major influence on susceptibility and progression of infectious diseases [33]
Summary
The human immunodeficiency virus infection (HIV) is essentially an infection of the immune system, with progressive and profound defects in the cell-mediated immune response, in which viral and host genetic factors may have an important role [1, 2]. HLA class I molecules play a major role in the immune response against viral infections and transformed cells by presenting peptide antigens to cytotoxic T lymphocytes (CTL). CTLs are major effectors in the cellular arm of antigen-specific immune responses They play a major role in protection and recovery from viral infection, mediate allograft rejection, are implicated in certain autoimmune diseases, and contribute to protection and recovery from certain bacterial and parasitic infections and to tumor immunity. The recognition and subsequent lysis of virus-infected target-host cells by CTL requires mediation by HLA class I molecules loaded with viral antigen-derived peptides on the cell surface. This HLA class I antigen-peptide complex is transported to the cell surface and is recognized by CTLs as a signal of virus infection, cancer, or autoimmune disease and destroy the diseased cell [6, 7]
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