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Early natural killer cell responses in hepatitis C virus exposed health-care workers who do not develop acute infection

Wednesday, October 26, 2011 — Poster Session III

10:00 a.m. – Noon

Natcher Conference Center




  • JM Werner
  • T Heller
  • B Rehermann


Acute hepatitis C virus (HCV) infection typically results in chronic disease with HCV outpacing adaptive immune responses. Here we asked whether innate responses of natural killer (NK) cells contribute to antiviral immunity in 12 prospectively studied health-care workers (HCWs) who were accidentally exposed to HCV via needlestick (n=10) or cut (n=2) but did not develop acute HCV infection. All HCWs remained HCV RNA and anti-HCV negative at all study time points. Peripheral blood NK cells responded to the exposure with peak expression of the activation markers CD122 at week 2, the activating receptors NKp44 and NKp46 at week four and the inhibitory receptor NKG2A at week six after exposure. NK cell cytotoxicity (degranulation and TRAIL expression) peaked at week four, and IFN-g production at week six. The multifunctional NK cell response of these HCV-exposed and protected HCW differed from the polarized NK cell response (increase in cytotoxicity and decrease in IFN-g production) typically seen in individuals with persistent infection. Furthermore, the increase in NK cell cytotoxicity correlated to the magnitude of the subsequent HCV-specific T cell response. These results suggest that NK cells contribute to the prevention of acute hepatitis and to the induction of adaptive immunity.

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