is through the level of NK subset IFN-aR expression that de-
termines IFN-a–induced signaling magnitude, in turn leading
to enhanced NKp30 (and other modulators of effector function),
which in turn contribute to control of HCV infection. Certainly,
NKp30 expression during IFN-a therapy has recently been
shown to associate with favorable response to therapy [20, 21].
Although this is a small data set, clearly, further investigation
of this NK subset is warranted, with speciﬁc emphasis on in-
vestigation of genetically encoded and environmental factors
contributing to enhanced IFN-aR expression and mechanisms
underlying downstream associations with magnitude of viral
Supplementary materials are available at The Journal of Infectious Diseases
online (http://www.oxfordjournals.org/our_journals/jid/). Supplementary
materials consist of data provided by the author that are published to beneﬁt
the reader. The posted materials are not copyedited. The contents of all
supplementary data are the sole responsibility of the authors. Questions or
messages regarding errors should be addressed to the author.
Acknowledgments. We thank the study participants, and Laura Napo-
litano, Yolanda Lie, and Eoin Coakley at Monogram Biosciences for helping
to make IL-28B genotyping possible.
Financial support. This work was supported by the National Institutes
of Health (grant numbers R01 DK068361 and R01 AI069195).
Potential conﬂicts of interest. All authors: No reported conﬂicts.
All authors have submitted the ICMJE Form for Disclosure of Potential
Conﬂicts of Interest. Conﬂicts that the editors consider relevant to the
content of the manuscript have been disclosed.
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