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Journal of Virology, February 2003, p. 2321-2329, Vol. 77, No. 4
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.4.2321-2329.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The Amino-Terminal Extensions of the Longer Sendai Virus C Proteins Modulate pY701-Stat1 and Bulk Stat1 Levels Independently of Interferon Signaling

Dominique Garcin,1 Jean-Baptiste Marq,1 Stephen Goodbourn,2 and Daniel Kolakofsky1*

Department of Genetics and Microbiology, University of Geneva School of Medicine, Centre Médicale Universitaire, CH1211 Geneva, Switzerland,1 Department of Biochemistry and Immunology, St. George's Hospital Medical School, University of London, London SW17 0RE, United Kingdom2

Received 5 September 2002/ Accepted 15 November 2002

The Sendai virus (SeV) C proteins are known to interact with Stat1 to prevent interferon (IFN)-induced pY701-Stat1 formation and IFN signaling. Nevertheless, pY701-Stat1 levels paradoxically increase during SeV infection. The C proteins also induce bulk Stat1 instability in some cells, similar to rubulavirus V proteins. We have found that SeV infection increases pY701-Stat1 levels even in cells in which bulk Stat1 levels strongly decrease. Remarkably, both the decrease in bulk Stat1 levels and the increase in pY701-Stat1 levels were found to be independent of the IFN signaling system, i.e., these events occur in mutant cells in which various components of the IFN signaling system have been disabled. Consistent with this, the C-induced decrease in Stat1 levels does not require Y701 of Stat1. We present evidence that C interacts with Stat1 in two different ways, one that prevents IFN-induced pY701-Stat1 formation and IFN signaling that has already been documented, and another that induces pY701-Stat1 formation (while decreasing bulk Stat1 levels) in a manner that does not require IFN signaling. These two types of Stat1 interaction are also distinguishable by C gene mutations. In particular, the IFN signaling-independent Stat1 interactions specifically require the amino-terminal extensions of the longer C proteins. The actions of the SeV C proteins in counteracting the cellular antiviral response are clearly more extensive than previously appreciated.

* Corresponding author. Mailing address: Dept. 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 5702. E-mail: Daniel.Kolakofsky{at}medecine.unige.ch.

Journal of Virology, February 2003, p. 2321-2329, Vol. 77, No. 4
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.4.2321-2329.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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