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Journal of Virology, September 1998, p. 7703-7706, Vol. 72, No. 9
Host Defense Laboratory, Viral Engineering
and Cytokines Group, Division of Immunology and Cell Biology, The
John Curtin School of Medical Research, The Australian National
University, Canberra, ACT 2601, Australia,1 and
Beatrice and Samuel A. Seaver Laboratory, Department of
Medicine, Cornell University Medical College, New York, New York
100212
Received 28 May 1998/Accepted 17 June 1998
To assess whether nitric oxide synthase 2 (NOS2) fulfills the criteria of an innate resistance locus
against an acute viral infection, we inoculated genetically deficient
NOS2
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Identification of Nitric Oxide Synthase
2 as an Innate Resistance Locus against Ectromelia Virus
Infection
/
mice with virulent ectromelia virus (EV), the causative agent
of mousepox. NOS2
/
mice proved highly susceptible to EV yet showed
no diminution in other well-characterized anti-EV immune responses,
i.e., gamma interferon secretion and NK cell and EV-specific cytotoxic
T lymphocyte activities. Thus, the NOS2 locus can be
considered a critical monogenic determinant of EV resistance
that contributes to host survival.
*
Corresponding author. Mailing address: Division of
Immunology and Cell Biology, The John Curtin School of Medical
Research, The Australian National University, P.O. Box 334, Canberra,
ACT 2601, Australia. Phone: 61 2 6249 2627. Fax: 61 2 6249 2595. E-mail: Guna.Karupiah{at}anu.edu.au.
Present address: Laboratory of Immunology, HHMI, The
Rockefeller University, New York, NY 10021.
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