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

Alterations of the NK cell pool in HIV/HCV co-infection.
Author Information (click to view)

Kaczmarek DJ, Kokordelis P, Krämer B, Glässner A, Wolter F, Goeser F, Lutz P, Schwarze-Zander C, Boesecke C, Strassburg CP, Rockstroh JK, Spengler U, Nattermann J,


Kaczmarek DJ, Kokordelis P, Krämer B, Glässner A, Wolter F, Goeser F, Lutz P, Schwarze-Zander C, Boesecke C, Strassburg CP, Rockstroh JK, Spengler U, Nattermann J, (click to view)

Kaczmarek DJ, Kokordelis P, Krämer B, Glässner A, Wolter F, Goeser F, Lutz P, Schwarze-Zander C, Boesecke C, Strassburg CP, Rockstroh JK, Spengler U, Nattermann J,

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PloS one 2017 04 0512(4) e0174465 doi 10.1371/journal.pone.0174465

Abstract
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.

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