Chemokine RANTES promoter polymorphism affects risk of both HIV infection and disease progression in the Multicenter AIDS Cohort Study

Abstract

These data implicate the RANTES-403A allele as a risk factor for HIV transmission and as a protective factor for HIV progression.

RANTES Gene Promoter Polymorphisms Are Associated with Bronchial Hyperresponsiveness in Korean Children with Asthma

“…In addition, the frequency of the RANTES -28G allele for the Korean children in our study was 18.7% higher than Japanese (16.6%) [14] or Chinese (11.7%) [17]. In Caucasians, the RANTES -28G allele was reported to be relatively uncommon (4%) [31]. Yao et al [17] asserted that RAN-TES polymorphisms might have a more substantial impact on the phenotype of asthma in the Asian population.…”

Global human genetics of HIV-1 infection and China

“…However, homozygous CCR5-32 has not been identified and heterozygous CCR5-32 is extremely rare in Chinese populations, indicating no or little effect of CCR5-32 on HIV-1 transmission and epidemic in China. Genetic polymorphisms that have been shown to influence HIV-1 transmission are relatively rare and only account for the resistance of a small proportion of ES individuals to infection [32,[45][46][47][48][49][50][51][52][53][54], underscoring the need for more research.…”

“…The -403A-28G haplotype was shown to be associated with delayed disease progression in HIV-1 infected Japanese, but exerts no influence on the incidence of HIV-1 infection [52]. In European-Americans, the compound genotype -403G/A -28C/C was reported to be resistant to AIDS progression in one study [53], but not in another [54]. These RANTES polymorphisms have no effect on HIV-1 infection and disease progression in African-Americans [54].…”

“…Significant studies in the past few years have also demonstrated that innate immunity including genetic polymorphisms in host genes can affect the risk for HIV-1 infection and disease progression (Tab. 1), although the effect of these alleles has been inconsistent [32,[45][46][47][48][49][50][51][52][53][54][55] (reviewed in [56]). Here, we review global and Chinese studies on human genetic polymorphisms and their association with HIV-1 infection.…”

Variants of CCR5, which are permissive for HIV-1 infection, show distinct functional responses to CCL3, CCL4 and CCL5

“…The exact CCR5 domains involved in gp41-mediated fusion have not been fully characterized, but modeling studies suggest that extracellular loop 2 and TM domain 5 may participate based on molecular models of the TAK-779 inhibitor interacting with CCR5 and epitope mapping studies. 49,50 From the point of view of the HIV epidemic, the low genetic frequency of these three variants (p0.016 or less), 34 and the wide genetic and phenotypic differences that regulate production of CCL3, CCL3L1, CCL4, CCL4L1 and CCL5, 8,10,11,51,52 make it difficult to predict the net effects of individual variants on viral infection and immune function. Although these CCR5 variants may not have a significant effect on the HIV pandemic, knowledge of their existence, impact on coreceptor function and interaction with coreceptor inhibitors will become useful tools to manage individual patient therapies as coreceptor inhibitors become more prominent anti-viral therapies.…”