CCR5 increment 32 and SDF1 3′A: Gene Variants, Expression and Influence on Biological Markers for the Clinical Progression to AIDS among HIV-1 Virus Controllers in a Mixed Population of the Amazon Region of Brazil

CCR5 Delta 32 and SDF1-3 ' A polymorphisms were investigated in a cohort of viremia controllers, without the use of therapy, along with their influence on CD4+ T lymphocytes (TLs), CD8+ TLs, and plasma viral load (VL). The samples were analyzed from 32 HIV-1-infected individuals classified as viremia controllers 1 and 2 and viremia non-controllers, from both sexes, mostly heterosexuals, paired with 300 individuals from a control group. CCR5 increment 32 polymorphism was identified by PCR amplification of a fragment of 189 bp for the wild-type allele and 157 bp for the allele with the increment 32 deletion. SDF1-3 ' A polymorphism was identified by PCR, followed by enzymatic digestion (restriction fragment length polymorphism) with the Msp I enzyme. The relative quantification of gene expression was performed by real-time PCR. The distribution of allele and genotype frequencies did not show significant differences between the groups. The gene expression of CCR5 and SDF1 was not different between the profiles of AIDS progression. There was no significant correlation between the progression markers (CD4+ TL/CD8+ TL and VL) and the CCR5 increment 32 polymorphism carrier status. The 3 ' A allele variant was associated with a marked loss of CD4+ TLs and a higher plasma VL. Neither CCR5 increment 32 nor SDF1-3 ' A was associated with viremia control or the controlling phenotype.

Automated summary

This study investigated the effects of CCR5 Delta 32 and SDF1-3 'A polymorphisms on viremia controllers. However, no significant differences were found between the groups. The expression of CCR5 and SDF1 genes was also not associated with AIDS progression. Interestingly, the 3'A allele variant was associated with a marked loss of CD4+ TLs and a higher plasma viral load.