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Journal of Virology, June 1999, p. 5196-5200, Vol. 73, No. 6
Department of
Neurology,1 Division of
Biology,2 and Division of
Biostatistics,3 Beckman Research Institute,
City of Hope National Medical Center, Duarte, California 91010
Received 15 December 1998/Accepted 22 February 1999
Mouse strains with null mutations in the gamma interferon gene
(Ifng) or the gamma interferon receptor gene
(Ifngr) have been engineered. The use of these strains as
animal models of viral and bacterial infections has enhanced our
understanding of the role of gamma interferon (IFN-
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Gamma Interferon (IFN-
) Receptor Null-Mutant
Mice Are More Susceptible to Herpes Simplex Virus Type 1 Infection
than IFN-
Ligand Null-Mutant Mice
) in the host
immune response. However, direct comparisons between
Ifng
/
(GKO) and Ifngr
/
(RGKO) mice have
been problematic because previously available strains of these mice
have had different genetic backgrounds (i.e., C57BL/6 and BALB/c for
GKO mice and 129/Sv//Ev for RGKO mice). To enable direct comparison of
herpes simplex virus type 1 (HSV-1) infections in GKO and RGKO mice, we
introduced the IFN-
null mutation into the 129/Sv//Ev background. We
report that, after HSV-1 inoculation, mortality was significantly
greater in RGKO mice than in GKO mice (38 versus 23%,
P = 0.0001). Similarly, the mortality from vaccinia
virus challenge was significantly greater in RGKO mice than in GKO
mice. With differences in genetic background excluded as a confounding
issue, these results are consistent with the existence of an
alternative ligand(s) for the IFN-
receptor that is also capable of
mediating protection against viral challenge.
*
Corresponding author. Mailing address: City of Hope
Medical Center, Department of Neurology, 1500 E. Duarte Rd., Duarte, CA 91010. Phone: (626) 301-8480. Fax: (626) 301-8852. E-mail:
ecantin{at}coh.org.
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