Abstract
BackgroundA 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.MethodsA 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.ResultsNK 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.ConclusionsOur 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.
Highlights
Due to similar transmission routes of infection a relevant proportion of human immunodeficiency virus (HIV)-positive patients is co-infected with the hepatitis C virus (HCV)[1]
HIV/HCV co-infection was associated with significantly decreased expression of the maturation/differentiation markers CD27/62L/ 127 on natural killer (NK) cells but increased expression of CD57 compared to healthy controls
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
Summary
Due to similar transmission routes of infection a relevant proportion of human immunodeficiency virus (HIV)-positive patients is co-infected with the hepatitis C virus (HCV)[1]. Persistent dysregulation of the natural killer (NK) cell pool is of especial interest, as NK cells have been shown to effectively block HCV replication[13,14] and to display an antifibrotic activity[15] Both HIV and HCV mono-infection are associated with significant perturbations of NK cells. A reduction of absolute NK cell numbers was found in HIV(+) as well as in HCV(+) patients[16,17] and both HIV and HCV mono-infection as well as HIV/HCV coinfection have been observed to be associated with the appearance of a highly dysfunctional subset of CD56- CD16+ NK cells, characterized by a poor cytotoxic activity[18,19,20,21,22,23] Both viral infections are characterized by altered expression patterns of activating NK cell receptors (NKR)[11,24,25] reports on NKR expression in chronic hepatitis C are controversial[24,25,26,27,28,29,30,31]. Little data is available concerning phenotype and function of NK cells in HIV/HCV co-infection
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