Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
2.
AIDS Res Hum Retroviruses ; 31(7): 685-91, 2015 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-25825809

RESUMO

Genetic factors from an HIV-1 host can affect the rate of progression to AIDS and HIV infection. To investigate the frequency of mutations in the CCR5 gene, HIV-1 samples from infected women and uninfected individuals were selected for sequencing of the CCR5 gene regions encoding the N- and C-terminal protein domains. Physicochemical CCR5 modeling and potential protein domain analysis were performed in order to evaluate the impact of the mutations found in the properties and structure of CCR5. The p.L55Q mutation in the N-terminal protein domain was observed only in uninfected individuals, with an allelic frequency of 1.8%. Physicochemical analysis revealed that the p.L55Q mutation magnified the flexibility and accessibility profiles and the modeling of CCR5 structures showed resulting in a small deviation to the right, as well as a hydrophobic to hydrophilic property alteration. The p.L55Q mutation also resulted in a slight modification of the electrostatic load of this region. Additionally, three novel silent mutations were found at the C-terminal coding region among HIV-1-infected women. The results suggest that the p.L55Q mutation might alter CCR5 conformation. Further studies should be conducted to verify the role of this mutation in HIV-1 susceptibility.


Assuntos
Infecções por HIV/genética , Proteínas Mutantes/genética , Mutação , Receptores CCR5/genética , Receptores de HIV/genética , Adulto , Idoso , Brasil , Fenômenos Químicos , Feminino , Frequência do Gene , HIV-1 , Humanos , Interações Hidrofóbicas e Hidrofílicas , Masculino , Pessoa de Meia-Idade , Modelos Moleculares , Proteínas Mutantes/química , Conformação Proteica , Receptores CCR5/química , Receptores de HIV/química , Adulto Jovem
3.
PLoS One ; 7(5): e37283, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22662140

RESUMO

The 7th cholera pandemic reached Latin America in 1991, spreading from Peru to virtually all Latin American countries. During the late epidemic period, a strain that failed to ferment sucrose dominated cholera outbreaks in the Northern Brazilian Amazon region. In order to understand the genomic characteristics and the determinants of this altered sucrose fermenting phenotype, the genome of the strain IEC224 was sequenced. This paper reports a broad genomic study of this strain, showing its correlation with the major epidemic lineage. The potentially mobile genomic regions are shown to possess GC content deviation, and harbor the main V. cholera virulence genes. A novel bioinformatic approach was applied in order to identify the putative functions of hypothetical proteins, and was compared with the automatic annotation by RAST. The genome of a large bacteriophage was found to be integrated to the IEC224's alanine aminopeptidase gene. The presence of this phage is shown to be a common characteristic of the El Tor strains from the Latin American epidemic, as well as its putative ancestor from Angola. The defective sucrose fermenting phenotype is shown to be due to a single nucleotide insertion in the V. cholerae sucrose-specific transportation gene. This frame-shift mutation truncated a membrane protein, altering its structural pore-like conformation. Further, the identification of a common bacteriophage reinforces both the monophyletic and African-Origin hypotheses for the main causative agent of the 1991 Latin America cholera epidemics.


Assuntos
Cólera/epidemiologia , Epidemias , Genoma Bacteriano , Sacarose/metabolismo , Vibrio cholerae/genética , Vibrio cholerae/metabolismo , Bacteriófagos/classificação , Bacteriófagos/genética , Composição de Bases , DNA Viral , Sequências Repetitivas Dispersas , América Latina/epidemiologia , Mutação , Fenótipo , Filogenia , Vibrio cholerae/virologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...