RESUMEN
BACKGROUND: Treatment failure of antiretroviral therapy in HIV-1 infection is increasing due to development of viral resistance. Trends of resistance-associated mutation lead to the ineffective treatment in HIV-infected individuals. METHODS: Extracted viral RNA from HIV-infected subjects in 2009 to 2010 was performed. The genotypic resistance testing was investigated for HIV-1 drug resistance in RT and PR genes. Frequencies of mutation were compared by a Fischer's exact test. RESULTS: Three hundred and sixty-nine samples (147 in 2009 and 222 in 2010) were genotyped. At least one mutation was found in 90.8% (335/369) in PR gene and 87.0% (321/369) in RT gene. Three sequences in PR gene, M36I, H69K, and L90M, were decreased significantly in 2010 when compared to 2009. Mutations associated with resistance to nucleoside analogue reverse transcriptase inhibitors (NRTI's) were found in 61.0% and 64.2% in nonnucleoside analogue reverse transcriptase inhibitors (NNRTI's). A total of 49.6% was found in combined NRTI and NNRTI. In 2010, M41L was increased significantly from 7.5% to 14.9%. However, there was a decrease in the frequency of the mutations at position 67, 70, and 184 between 2009 and 2010. CONCLUSIONS: In 2010, three mutations in PR gene, M36I, H69K, and L90M, were decreased significantly. However, only one mutation in RT gene, M41L was significantly increased.
Asunto(s)
Farmacorresistencia Viral/genética , Infecciones por VIH/tratamiento farmacológico , VIH-1/efectos de los fármacos , VIH-1/genética , Adulto , Anciano , Fármacos Anti-VIH/uso terapéutico , Terapia Antirretroviral Altamente Activa , Femenino , Frecuencia de los Genes , Genotipo , Infecciones por VIH/virología , Humanos , Masculino , Pruebas de Sensibilidad Microbiana , Persona de Mediana Edad , Mutación , Tasa de Mutación , Prevalencia , ARN Viral/genética , Inhibidores de la Transcriptasa Inversa/uso terapéutico , Tailandia , Insuficiencia del Tratamiento , Carga Viral , Adulto JovenRESUMEN
BACKGROUND: The genotypic polymorphisms of CCR5, CCR2, and SDF1 were analyzed to determine their impact as potential confounders with regard to disease progression because of the role that host genetic factors appear to be involved in determining rates of disease progression. METHODS: Genomic DNA was extracted from Ethylenediaminetetraacetate whole blood using Qiagen DNA extraction kit. The amplification of CCR5, CCR2, and SDF1 genes was performed by PCR. RESULTS: Two hundred and twenty-one samples were genotyped for the CCR5, CCR2, and SDF1 mutation. Among these, all (100%) were identified as wild type for CCR5. All were then investigated considering the impact on CD4+ T-cell counts. Samples were divided into two groups based on the CD4+ T-cell numbers. It revealed that in the group of CD4+ T-cell counts ≥200 cells/µl, 15 were found for the homozygous for SDF1 gene (3'A/3'A) whereas one was found in the group of CD4+ T-cell counts <200 cells/µl. Homozygosity for the CCR2 polymorphisms (64I/64I) were five in the group of CD4+ T-cell counts ≥200 cells/µl and none were found in the group of CD4+ T-cell counts <200 cells/µl. These results demonstrated that there was a significant association between CD4+ T-cell numbers and CCR2 and SDF1 polymorphisms (P < 0.001). CONCLUSIONS: The mutation of CCR2 and SDF1 genes showed a significant difference in the distribution of CD4+ T-cell numbers (P < 0.001) whereas mutation of chemokine coreceptor CCR5 was not appeared to be associated with the impact of CD4+ T-cell counts.