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

Bases de dados
Ano de publicação
Tipo de documento
País de afiliação
Intervalo de ano de publicação
1.
Curr HIV Res ; 18(3): 194-200, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32209045

RESUMO

BACKGROUND: Coinfection of Hepatitis C virus (HCV) with human immunodeficiency virus (HIV) has a higher risk of mortality than HCV or HIV monoinfection. HCV and HIV infections are specified by systemic inflammation, but the inflammation process in HCV/HIV coinfection is much complicated and is not well characterized. OBJECTIVE: The aim of this study was to analyze the expression of TLR-3, TLR-7, IL-10, IFN-1 (IFN-α, IFN-ß), and TNF-α in HIV, HCV and HIV/HCV co-infected patients. METHODS: Forty-five patients including HIV group (n=15), HCV group (n=15), HIV/HCV coinfection group (n=15) and healthy control group (n=15) participated. Peripheral blood mononuclear cells (PBMCs) were obtained. PBMC-RNA, HCV and HIV RNA were extracted from all subjects and cDNA was synthesized. The viral load analyzed by reverse transcription-quantitative PCR (RT-qPCR), and the expression levels of IFN-α, IFN-ß, TLR-3, TLR-7, TNF, and IL-10 mRNA were quantified in PBMCs. RESULTS: The levels of IFN-I, IL-10, and TNF-α were overexpressed in all patients' groups (p<0.05), TLR-7 was upregulated in all groups, but this upregulation was not statistically significant (p>0.05). TLR-3 showed a decrease in all patient groups (p<0.05). The statistical analysis demonstrated that TLR-3 has a negative correlation with HIV load, whereas other genes positively correlated with HIV load. In addition, TLR-3, TNF-α, and IFN-I were negatively correlated with HCV load, whereas TLR-7 and IL-10 s were positively correlated with HCV load. CONCLUSION: Our results showed a significant relationship between the expression level of innate immunity genes and inflammation in HCV, HIV, and HIV/HCV coinfected patients.


Assuntos
Infecções por HIV/imunologia , HIV/imunologia , Hepacivirus/imunologia , Hepatite C Crônica/imunologia , Imunidade Inata , RNA Viral/imunologia , Adulto , Estudos de Casos e Controles , Coinfecção , Feminino , Regulação da Expressão Gênica , HIV/genética , Infecções por HIV/genética , Infecções por HIV/patologia , Infecções por HIV/virologia , Hepacivirus/genética , Hepatite C Crônica/genética , Hepatite C Crônica/patologia , Hepatite C Crônica/virologia , Interações Hospedeiro-Patógeno/genética , Interações Hospedeiro-Patógeno/imunologia , Humanos , Inflamação , Interferon-alfa/genética , Interferon-alfa/imunologia , Interferon beta/genética , Interferon beta/imunologia , Interleucina-10/genética , Interleucina-10/imunologia , Masculino , Pessoa de Meia-Idade , RNA Viral/genética , Receptor 3 Toll-Like/genética , Receptor 3 Toll-Like/imunologia , Receptor 7 Toll-Like/genética , Receptor 7 Toll-Like/imunologia , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/imunologia , Carga Viral/genética , Carga Viral/imunologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA