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Journal of Virology, August 2001, p. 6800-6807, Vol. 75, No. 15
Department of Genetics and Microbiology,
University of Geneva School of Medicine, CH1211 Geneva,
Switzerland,1 and Osaka Prefectural
Institute of Public Health, Higashinari, 537-0025 Osaka,
Japan2
Received 25 January 2001/Accepted 25 April 2001
The Sendai virus (SeV) C gene codes for a nested set of four C
proteins that carry out several functions, including the modulation of
viral RNA synthesis and countering of the cellular antiviral response.
Using mutant C genes (and in particular a C gene with a deletion of six
amino acids present only in the larger pair of C proteins) and
recombinant SeV carrying these mutant C genes, we find that the nested
set of C proteins carry out a nested set of functions. All of the C
proteins interdict interferon (IFN) signaling to IFN-stimulated genes
(ISGs) and prevent pY701-Stat1 formation. However, only the larger C
proteins can induce STAT1 instability, prevent IFN from inducing an
antiviral state, or prevent programmed cell death. Remarkably,
interdiction of IFN signaling to ISGs and the absence of pY701-Stat1
formation did not prevent IFN-
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.15.6800-6807.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Longer and Shorter Forms of Sendai Virus C Proteins Play
Different Roles in Modulating the Cellular Antiviral Response
from inducing an anti-Vesicular
stomatitis virus (VSV) state. It is possible that IFN-
signaling to
induce an anti-VSV state can occur independently of the
well-established Jak/Stat/ISGF3 pathway and that it is this parallel
pathway that is targeted by the longer C proteins.
*
Corresponding author. Mailing address: Department of
Genetics and Microbiology, University of Geneva School of Medicine,
CMU, 9 Ave. de Champel, CH1211 Geneva, Switzerland. Phone:
41-22-702-56-57. Fax: 41-22-702-57-02. E-mail:
Daniel.Kolakofsky{at}Medecine.unige.ch.
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