Volume 8 • Issue 1 • 1000653 Open Access Research Article J AIDS Clin Res, an open access journal ISSN: 2155-6113 Kakkar et al., J AIDS Clin Res 2017, 8:1 DOI: 10.4172/2155-6113.1000653 J o u r n a l o f A I D S & C l i n i c a l R e s e a r c h ISSN: 2155-6113 Journal of AIDS & Clinical Research Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population Kavita Kakkar 1,2 , Swati Sharma 1,2 , Anurag Rathore 1 , Satyendra K Singh 1 , Nikky Nyari 1 , Manoj Km Singh 3 , Tapan N Dhole 1* , Vikas Agarwal 4 , Sayali Mukherjee 2 and Naveen KM Srivastava 1 1 Department of Microbiology Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India 2 Amity Institute of Biotechnology, Amity University, Lucknow, India 3 National University of Science and Technology, MISiS, Moscow 4 Department of Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India *Corresponding author: Dr. Tapan N Dhole, MD, Department of Microbiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow-226014, India; Tel: +91-522-2494263; Fax: +91-522-2668100; +91-522-2668017; E-mail: tndhole@gmail.com Received November 15, 2016; Accepted January 06, 2017; Published January 13, 2017 Citation: Kakkar K, Sharma S, Rathore A, Singh SK, Nyari N, et al. (2017) Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population. J AIDS Clin Res 8: 653. doi: 10.4172/2155-6113.1000653 Copyright: © 2017 Kakkar K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Keywords: AIDS; Apolipoprotein; Cytidine deaminase; HIV; Disease susceptibility Introduction Human immunodefciency virus (HIV) is the cause of Acquired Immuno Defciency Syndrome (AIDS) infection, that targets the immune system guiding to a state of immunodefciency in setting of immune activation, and the course of the disease is deeply infuenced by inter-individual variability [1]. Te acute phase of HIV infection is characterized by a substantial drop in CD4+ T cell count [2,3]. Te APOBEC (Apolipoprotein B mRNA-editing enzyme-catalytic polypeptide) serves as a shield to retro elements [4] belonging to cytidine deaminases family [5], comprising of seven host restriction factors (APOBEC3A-H) and has the ability to edit DNA/RNA which constitute an innate barrier to retroviruses, endogenous retro-elements and DNA viruses [6-8] and thus functions as DNA mutators, thereby, forming an important part of immune system, acting in both adaptive and innate immunity [9]. Tese cytidine deaminases object the genome of both the host and its invading pathogens [10]. APOBEC3 genes are located on chromosome 22 [11] and these proteins acts upon viral nucleic acids as a form of intrinsic host defense [12]. A3 (APOBEC3) enzymes are capable of editing single-stranded DNA and recognize specifc target sequences [13-16]. It plays an important role in the innate immune system and acts upon host defense against exogenous viruses and endogenous retro elements [17-20]. For HIV-1 to successfully infect humans, it must overcome numerous physical and immunological barriers [21,22]. Within cells, HIV must overcome a network of restriction factors that are able to block specifc replication steps of the virus, including A3 Enzymes [23]. Viral infectivity factor (Vif) plays a role in HIV-1 to overcome A3 enzymes [13,23-26]. By disrupting the Vif–host cell interactions through novel pharmaceuticals, A3 enzymes can be used to suppress HIV-1 infection. APOBEC3B is resistant to Vif-mediated degradation [16] and is able to suppress the infectivity of both Vif-defcient and wild-type HIV-1 with equal efciency [27]. Tese in vitro evidences suggest APOBEC3B as a potential strong inhibitor of HIV-1 in vivo. A segment spanning 29.5 kb between the ffh exon of APOBEC3A and eighth exon of APOBEC3B in chromosome 22 is deleted, which is frequently present among Asians [11]. Previous studies shows that the rate of progression of the disease Abstract Objective: Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-Like 3B (APOBEC3B) is involved in innate immune response, exhibiting insertion–deletion polymorphism across the world in human population. A naturally occurring 29.5 kb deletion removes complete APOBEC3B gene. Human APOBEC3B family of proteins restricts HIV- 1 replication. Very few studies have been conducted on this subject and the deductions regarding the effects of APOBEC3B deletion on HIV-1 susceptibility and pathogenesis have been largely inconsistent. Therefore, we studied the association of APOBEC3B deletion with HIV-1 in the North Indian population. Methods: Insertion (I)/Deletion (D) APOBEC3B polymorphism was analyzed using Polymerase chain reaction. Infection rates as wells as stages of HIV were compared among the three genotypes: deletion-homozygous (D/D), Insertion- homozygous (I/I) and hemizygous (I/D) in 150 HIV-1 seropositive (HSP) and 250 HIV-1 seronegative (HSN) subjects. Results and discussion: The genotypic analysis revealed insignifcant associations among homozygous deletion (D/D) genotype (P=0.130, OR=1.93, 95% CI=0.95–4.30) and moderate associations among hemizygous (I/D) genotypes (P=0.057, OR=1.56, 95% CI-1.03–2.44) with HIV-1 susceptibility and also the single copy of variant allele was more susceptible to HIV-1 infection. The severity of HIV-1 infection on the basis of CD4 count was not associated signifcantly with the disease progression to AIDS. Conclusion: In conclusion, we found that the deletion genotype of APOBEC3B gene polymorphism does not play any signifcant role on HIV-1 susceptibility. Hence, further studies with the expansion of sample size are needed to validate the results.