Expansion of CD56− NK cells in chronic HCV/HIV-1 co-infection: Reversion by antiviral treatment with pegylated IFNα and ribavirin

Abstract Co-infection with HCV and HIV-1 is a problem of increasing importance and the role of innate cellular immunity in this co-infection is incompletely understood. Here, we have observed sharply elevated numbers of CD56− CD16+ perforinlow NK cells in HCV/HIV-1 co-infected subjects on antiretrov...

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Published in:Clinical immunology (Orlando, Fla.) Fla.), 2008-07, Vol.128 (1), p.46-56
Main Authors: Gonzalez, Veronica D, Falconer, Karolin, Michaëlsson, Jakob, Moll, Markus, Reichard, Olle, Alaeus, Annette, Sandberg, Johan K
Format: Article
Language:English
Subjects:
Allergy and Immunology
Biological and medical sciences
CD1d
Fundamental and applied biological sciences. Psychology
Fundamental immunology
HCV
HIV
Human viral diseases
Infectious diseases
Interferon
Medical sciences
NK cells
NKT cells
Viral diseases
Viral diseases of the lymphoid tissue and the blood. Aids
Viral hepatitis
Viral infections
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Summary:Abstract Co-infection with HCV and HIV-1 is a problem of increasing importance and the role of innate cellular immunity in this co-infection is incompletely understood. Here, we have observed sharply elevated numbers of CD56− CD16+ perforinlow NK cells in HCV/HIV-1 co-infected subjects on antiretroviral therapy. Interestingly, this expansion of unconventional CD56− NK cells rapidly reverted when HCV was suppressed by IFNα and ribavirin treatment, and was not seen in mono-infected control groups. In vitro experiments suggested that this effect of treatment was due to suppression of HCV viremia rather than a direct effect of IFNα on these cells. In contrast, the conventional CD56+ NK cells were largely unchanged in subjects with high HCV loads, although they exhibited slightly decreased perforin expression. With delayed kinetics, the CD56bright immuno-regulatory NK cell subset temporarily increased to supranormal levels in response to HCV treatment. In contrast to the NK compartment, the CD1d-restricted NKT cells were severely reduced by the co-infection and not restored by treatment. Together, our data suggest that the high HCV loads in HCV/HIV-1 co-infection alter the NK cell compartment in a way not observed in HCV mono-infection.
ISSN:1521-6616
1521-7035
DOI:10.1016/j.clim.2008.03.521