Abstract

We attempted to study the role of HLA HLA-A, B, DRB1 and DQB1 in HIV-1 patient’s co infected with pulmonary tuberculosis (PTB). A total of 102 HIV-1 + patients co-infected with pulmonary tuberculosis and 200 healthy controls were included in HLA analysis. HLA-A*, HLA-B* HLA-DRB1* and DQB1* typing was done molecularly by PCR- SSOP (Polymerase Chain reaction-Sequence Specific Oligonucleotide Probing) method using kit (Dynal Kit – Invitrogen). The frequencies of the HLA-A, B HLA-DRB,1 and DQB1 alleles were determined using standard software. The HLA alleles identified among HIV + ve/PTB + ve co-infected patients as compared with healthy controls showed a significantly increased frequency of HLA-B*08:01:01 in HIV + ve/PTB + ve co-infected patients when compared with healthy controls (p = 0.011, OR 3.335, 95% CI 1.35-8.18), Likewise HLA-DQB1*03:01:03 was significantly increased in HIV + ve/PTB + ve co-infected patients as against healthy controls (p < 0.0001, OR 107.5, 95% CI 6.195 - 1865.3). Similarly HLA-DQB*06:01:02 allele frequency was observed in HIV + ve/PTB + ve co-infected patients as against healthy controls (p = 0.003, OR 4.808, 95% CI 1.72-13.39), HLA-DQB1*03:01:01 (p = 0.045, OR 0.219, 95% CI 0.051 - 0.940), HLA-DQB1*06:01:01:01 (p = 0.012, OR 0.334, 95% CI 0.145 - 0.770), alleles in HIV + ve/PTB + ve co-infected patients when compared with healthy controls. We can be concluded that different HLA alleles may render susceptibility or protection to in different ethnic population.

Highlights

  • Acquired immunodeficiency syndrome (AIDS) caused by HIV infection is endemic all over the globe and it is on the rise especially in resource limited countries

  • The HLA alleles identified among HIV+ve/pulmonary tuberculosis (PTB)+ve co-infected patients as compared with healthy controls showed a significantly increased frequency of HLA-B*08:01:01 in HIV+ve/PTB+ve co-infected patients when compared with healthy controls (p = 0.011, OR 3.335, 95% CI 1.35 - 8.18), Likewise HLA-DQB1*03:01:03 was significantly increased in HIV+ ve/PTB+ve co-infected patients as against healthy controls (p < 0.0001, OR 107.5, 95% CI 6.195 - 1865.3)

  • HLA-DQB*06:01:02 allele frequency was observed in HIV + ve/PTB + ve co-infected patients as against healthy controls (p = 0.003, OR 4.808, 95% CI 1.72 - 13.39), HLA-DQB1*03:01:01 (p = 0.045, OR 0.219, 95% CI 0.051 - 0.940), HLA-DQB1*06:01:01:01 (p = 0.012, OR 0.334, 95% CI 0.145 - 0.770), alleles in HIV+ve/PTB+ve co-infected patients when compared with healthy controls

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Summary

Introduction

Acquired immunodeficiency syndrome (AIDS) caused by HIV infection is endemic all over the globe and it is on the rise especially in resource limited countries. Individuals with impaired cell mediated immunity due to AIDS have a greatly increased risk of co-infection with Mycobacterium tuberculosis [1,2]. The co-infection of HIV-1 and Mycobacterium tuberculosis causes two infectious diseases endangering human health significantly. The factors influencing the greater inter individual variability to susceptibility to PTB co-infection and progression of AIDS is yet to be identified. This may be due to considerable varied immune responses of HIV-1 and MTB exposed individuals may result from the different genetic background. MHC class-I restricted CD8+ T cells are important for the generation of protective immune response in Mycobacterium tuberculosis infection. CD8+ CTL (Cytotoxic T lymphocytes)—derived IFN- may be especially important both for cells lacking MHC class-II molecules

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