ABSTRACT
OBJETIVO: Establecer la frecuencia y la relación del alelo CCR5-Δ32 con la infección y la progresión clínica de pacientes VIH+ y en individuos expuestos seronegativos. MATERIAL Y MÉTODOS: Se analizaron 355 muestras, 62 VIH+, 51 individuos expuestos seronegativos y 242 de la población general. Los VIH+ se subdividieron en: a) progresores normales n= 49; b) progresores lentos n= 10, y c) no progresores n= 3. RESULTADOS: Se identificó el genotipo wt/Δ32 en 17.7 por ciento de los VIH+, 13.7 por ciento de los individuos expuestos seronegativos y 6.2 por ciento en la población general. El genotipo Δ32/Δ32 se encontró en 3.9 por ciento de los individuos expuestos seronegativos. Según la progresión clínica de los VIH+, se identificó el genotipo wt/Δ32 en 10.2 por ciento de los progresores normales, 30 por ciento de los progresores lentos y en 100 por ciento de los no progresores. CONCLUSIÓN: El genotipo wt/Δ32 se observó en todos los no progresores, lo que apoya su papel en esta forma de progresión clínica en este grupo.
OBJECTIVE: CCR5-Δ32 allele frequency needs to be identified in HIV+ patients and exposed seronegative individuals in Yucatan, Mexico, to understand this mutation's relationship to infection and disease progression. MATERIAL AND METHODS: A total of 355 samples were analyzed: 62 from HIV+ patients, 51 from exposed seronegative individuals and 242 from general population. Infected patients were subdivided into a) normal progressors n= 49; b) slow progressors n= 10, and c) non-progressors n= 3. RESULTS: Genotype wt/Δ32 was identified in 17.7 percent of HIV+, 13.7 percent of exposed seronegative individuals and 6.2 percent of general population. Genotype Δ32/Δ32 was identified in 3.9 percent of exposed seronegative individuals. In infected patients, wt/Δ32 was identified in 10.2 percent of normal progressors, 30 percent of slow progressors and 100 percent of non-progressors. CONCLUSION: Genotype wt/Δ32 was observed in all non-progressing HIV+ patients, supporting its role in this group's disease development and clinical evolution.
Subject(s)
Female , Humans , Male , Gene Frequency , HIV Seropositivity/genetics , /genetics , Cross-Sectional Studies , Disease Progression , Genotype , HIV Seronegativity/genetics , Mexico , Prospective Studies , /immunologyABSTRACT
The present study investigated the prevalence of mutations in the -550 (H/L) and -221 (X/Y) mannose-binding lectin (MBL) gene promoter regions and their impact on infection by human immunodeficiency virus 1 (HIV-1) in a population of 128 HIV-1 seropositive and 97 seronegative patients. The allele identification was performed through the sequence-specific primer polymerase chain reaction method, using primer sequences specific to each polymorphism. The evolution of the infection was evaluated through CD4+ T-lymphocyte counts and plasma viral load. The allele and haplotype frequencies among HIV-1-infected patients and seronegative healthy control patients did not show significant differences. CD4+ T-lymphocyte counts showed lower levels among seropositive patients carrying haplotypes LY, LX and HX, as compared to those carrying the HY haplotype. Mean plasma viral load was higher among seropositive patients with haplotypes LY, LX and HX than among those carrying the HY haplotype. When promoter and exon 1 mutations were matched, it was possible to identify a significantly higher viral load among HIV-1 infected individuals carrying haplotypes correlated to low serum levels of MBL. The current study shows that haplotypes related to medium and low MBL serum levels might directly influence the evolution of viral progression in patients. Therefore, it is suggested that the identification of haplotypes within the promoter region of the MBL gene among HIV-1 infected persons should be further evaluated as a prognostic tool for AIDS progression.