Human APOBEC3 (A3) cytidine deaminases constitute cellular intrinsic defense mechanism, inhibiting replication of
retroviruses acting in both innate and adaptive pathways. A3B exhibit insertion/deletion (I/D) polymorphism providing
immunity to retroviral infection. In humans, high-frequency distribution of 29.5 kb deletion occurs and A3B deletion genotype
results in complete loss of A3B coding region. IL-16, a proinflammatory cytokine, activates T-cells by binding to CD4. Recently,
SNP involving T/C substitution at position 295 has been described. This study investigated the effect of I/D and IL-16 (295
T/C) polymorphism on susceptibility to HIV among 84 HIV seronegative (HSN) and 26 HIV seropositive (HSP) individuals
in North Indian population, which was assessed based on frequencies of genotypes: deletion-homozygous (D/D), hemizygous
(D/I), no deletion (I/I) and IL 16 (295 T/C) between infected and uninfected cohorts. Genotypic Frequencies showed no
significant difference between HSP and HSN of A3B (I/I 57.7%, I/D 30.8% and D/D 11.5%) (I/I 42.9%, I/D 30.9% and D/D
26.2%) and IL16 (295) (T/T 88.5%, T/C 7.7%, C/C 3.8%) (T/T 82%, T/C 9.5%, C/C 8.3%). Also no association of deletion
allele was observed in HSN (I vs D: OR = 0.327, p = 0.093, 95% CI= 0.085-1.26 and I vs I/D: OR = 0.738, p = 0.550, 95% CI =
0.273-1.9) compared with HSP. Herein, preliminary analysis of our data shows no significant impact of A3B deletion and IL
16 polymorphism in the predisposition of HIV-1 susceptibility. Further val