IL-18 GENE PROMOTER REGION 607C/A POLYMORPHISM IN HIV-1 INFECTED NORTH INDIAN POPULATION
Sobti RC1,*, Sharma VL2, Abitew AM2, Berhane N1, Mahdi SA1, Askari M1, Kuttiat VS3, Wanchu A3
*Corresponding Author: Ranbir C. Sobti, Department of Biotechnology, Panjab University, Chandigarh 160 014 India; Tel.: +172-2534087; +94-1-704-4523; Fax: +172-25341409; E-mail: rcsobti@ pu.ac.in
page: 41

INTRODUCTION

Human immunodeficiency virus type 1 (HIV-1) infection results in progressive deterioration of the immune system and in acquired immune deficiency syndrome (AIDS). However, the rate at which the HIV-1 infection progresses to AIDS varies considerably between individuals, some progressing rapidly after primary infection, while others remain asymptomatic with no evidence of immune dysfunction for over 15 years [1,2]. The reasons for the variation are multifactorial and may involve genetic, virological or immunological factors that function in different ways [3]. The role of host genetic variations has been intensively examined in different populations and in all major risk groups. These have revealed that genetic polymorphisms in genes for chemokine receptors or in those of their natural ligands are likely to influence susceptibility or resistance to HIV-1 infection as well as the subsequent rate of disease progression [3,4]. Genes for human leukocyte antigens (HLA) that regulate host immune response to infection have also been correlated with the clinical course of HIV-1 infection [5]. So far, in addition to polymorphic variants in genes encoding for HIV-1 co-receptors and their ligands and those of HLA alleles, some T helper type 1 (Th1) and type 2 (Th2) cytokine genes have also been implicated to influence the rate of disease progression in HIV-1 seropositive patients either positively or negatively [6,7]. Cytokines play a crucial role in regulation of the balance between Th1 and Th2 immune responsiveness. The Th1 cytokines promote cell-mediated immunity to intracellular pathogens including viruses and other intracellular pathogens, whereas Th2 cytokines enhance humoral immunity by up-regulating antibody production against extracellular pathogens [8,9]. Furthermore, several cytokine related studies confirmed their key immunomodulatory role within the immune system and cytokine genes have been targeted for association studies of susceptibility and development of several immune-related and infectious diseases [10-13]. The interleukin-18 (IL-18) gene encoding human IL-18 cytokine is located at chromosome 11q22.2- 22.3 [14,15]. Three single nucleotide polymorphisms (SNPs) (656G>T, 607C>A, 137G>C) within the IL-18 gene promoter have been localized. Of these, those at positions 137 and 607 influence the quantitative expression of the IL-18 protein. The 607C>A disrupts a potential cyclic adenosine monophosphate (cAMP) responsive element-binding protein (CREB) binding site and 137G>C abolishes the human histone 4 transcription factor-1 (H4TF-1)-binding site , reducing its transcription. Thus, these two polymorphisms and their haplotypes seem to account for differential IL-18 expression and changes in the production of this cytokine [15]. The multiple biological functions of the IL-18 gene are associated with a wide variety of allergic, inflammatory, autoimmune, cancerous and infectious diseases [16,17]. In the context of HIV-1 infection, the IL-18 cytokine also plays a pathogenic role by enhancing viral replication in monocytic cells and in T cells [18,19]. Moreover, clinical studies have demonstrated the involvement of IL-18 in the immunopathogenesis of HIV-1 infection [20-22]. However, most of these studies focused primarily on the association of the levels of IL-18 and the pathogenesis of HIV-1 infection. Several studies have examined the association of SNPs in the IL-18 gene with various other diseases [23,24], but that with the HIV-1 infection has not been fully explored. For this reason, we have evaluated the association of the IL-18 gene promoter polymorphism 607C>A with the HIV-1/AIDS infections. To the best of our knowledge, this is the first association study of the IL-18 gene polymorphism in North Indian HIV-1/ AIDS patients.



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