Your browser doesn't support javascript.

Portal de Pesquisa da BVS Enfermagem

Informação e Conhecimento para a Saúde

Home > Pesquisa > ()
XML
Imprimir Exportar

Formato de exportação:

Exportar

Email
Adicionar mais destinatários
| |

Alterations of the NK cell pool in HIV/HCV co-infection.

Kaczmarek, Dominik J; Kokordelis, Pavlos; Krämer, Benjamin; Glässner, Andreas; Wolter, Franziska; Goeser, Felix; Lutz, Philipp; Schwarze-Zander, Carolynne; Boesecke, Christoph; Strassburg, Christian P; Rockstroh, Jürgen K; Spengler, Ulrich; Nattermann, Jacob.
PLoS One ; 12(4): e0174465, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28380039

BACKGROUND:

A relevant proportion of human immunodeficiency virus (HIV) infected patients is co-infected with the hepatitis C virus (HCV). HCV co-infection in HIV-positive patients is associated with faster progression of liver disease in comparison to HCV mono-infection. Natural killer (NK) cells critically modulate the natural course of HCV infection. Both HIV and HCV mono-infection are associated with alterations of the NK cell pool. However, little data is available concerning phenotype and function of NK cells in HIV/HCV co-infection.

METHODS:

A total of 34 HIV/HCV co-infected, 35 HIV and 39 HCV mono-infected patients and 43 healthy control persons were enrolled into this study. All HIV-positive patients were under effective antiretroviral therapy. NK cell phenotype, IFN-γ production and degranulation were studied by flow cytometry.

RESULTS:

NK cell frequency in HIV/HCV co-infection was significantly lower than in healthy individuals but did not differ from HIV and HCV mono-infection. HIV/HCV co-infection was associated with significantly decreased expression of the maturation/differentiation markers CD27/62L/127 on NK cells but increased expression of CD57 compared to healthy controls. Of note, expression also differed significantly from HCV mono-infection but was similar to HIV mono-infection, suggesting a pronounced impact of HIV on these alterations. Similar findings were made with regard to the NK cell receptors NKG2A/C and NKp30. More importantly, NK cells in co-infection displayed a highly impaired functional activity with significantly lower IFN-γ production and degranulation than in healthy donors as well as HIV and HCV mono-infection, suggesting a synergistic effect of both viruses.

CONCLUSIONS:

Our data indicate that HIV/HCV co-infection is associated with significant alterations of the NK cell pool, which might be involved in the rapid progression of liver disease in co-infected patients and which mainly reflect alterations observed in HIV mono-infection.