Association of RANTES −403 G/A, −28 C/G and In1.1 T/C polymorphism with HIV-1 transmission and progression among North Indians
✍ Scribed by Anurag Rathore; Animesh Chatterjee; P. Sivarama; Naohiko Yamamoto; Pradeep K. Singhal; Tapan N. Dhole
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 96 KB
- Volume
- 80
- Category
- Article
- ISSN
- 0146-6615
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✦ Synopsis
Abstract
The relationships between host immune factors and HIV‐1 disease progression are still in dispute. The RANTES SNPs exhibit distinct ethnic distribution and are associated with different effects on the course of HIV infection. Therefore, impact of RANTES gene polymorphism on HIV‐1 transmission and progression needs to be evaluated. The RANTES genotypes were identified by PCR‐RFLP method and confirmed by sequencing in HIV‐1 seronegative (HSN; n = 315), HIV‐1 exposed seronegative (HES; n = 47) and HIV‐1 seropositive (HSP; n = 196) patients classified into different clinical stages (i.e. Stages I, II, III). Fisher exact test was used for statistical analysis and Arlequin software for haplotype analysis. RANTES allele −403G, −28C and In1.1 T were the predominant allele in the subject studied. HSP group have higher frequency of RANTES In1.1 T allele compared with HSN (91.32% vs. 86.19%; P = 0.013) and HES (91.32% vs. 78.72%; P = 0.001). Higher frequency of RANTES In1.1 C allele in Stage III was observed, compared with Stage I (14.28% vs. 6.39%) and was significantly associated with high risk (P = 0.047, OR = 2.439, C.I. = 1.061–5.609). Haplotype II (ACT) was significantly higher in HSP compared with HSN (9.69% vs. 1.58%) and associated with high risk (P < 0.001, OR = 6.655, C.I. = 2.443–18.132). There were no significant differences in RANTES −403 A/G and −28 C/G genotype and allele distribution in all the groups compared. Our results implicate that RANTES In1.1 T allele and haplotype II (ACT) may be a risk factor for HIV‐1 transmission while RANTES In1.1 C allele may be risk factor for disease progression among North Indians. J. Med. Virol. 80: 1133–1141, 2008. © 2008 Wiley‐Liss, Inc.
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