Cargando…

CCR5∆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

CCR5Δ32 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 contro...

Descripción completa

Detalles Bibliográficos
Autores principales: Lima, Érica Ribeiro Gomes, Queiroz, Maria Alice Freitas, Lima, Sandra Souza, Machado, Luiz Fernando Almeida, Cayres-Vallinoto, Izaura Maria Vieira, Vallinoto, Antonio Carlos Rosário, Figueiredo, Fernanda Andreza de Pinho Lott, Guerreiro, João Farias, Guimarães Ishak, Marluísa de Oliveira, Ishak, Ricardo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10003039/
https://www.ncbi.nlm.nih.gov/pubmed/36902388
http://dx.doi.org/10.3390/ijms24054958
Descripción
Sumario:CCR5Δ32 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∆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 ∆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∆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∆32 nor SDF1-3′A was associated with viremia control or the controlling phenotype.