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Journal of Virology, March 2007, p. 2554-2563, Vol. 81, No. 6
0022-538X/07/$08.00+0     doi:10.1128/JVI.01634-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Mouse Hepatitis Coronavirus A59 Nucleocapsid Protein Is a Type I Interferon Antagonist{triangledown}

Ye Ye,1,3,{dagger} Kevin Hauns,2,3,{dagger} Jeffrey O. Langland,3 Bertram L. Jacobs,3 and Brenda G. Hogue3*

The Biodesign Institute and School of Life Sciences,3 Microbiology Graduate Program,1 Molecular Cellular Biology Graduate Program, Arizona State University, Tempe Arizona 85287-54012

Received 31 July 2006/ Accepted 13 December 2006

The recent emergence of several new coronaviruses, including the etiological cause of severe acute respiratory syndrome, has significantly increased the importance of understanding virus-host cell interactions of this virus family. We used mouse hepatitis virus (MHV) A59 as a model to gain insight into how coronaviruses affect the type I alpha/beta interferon (IFN) system. We demonstrate that MHV is resistant to type I IFN. Protein kinase R (PKR) and the alpha subunit of eukaryotic translation initiation factor are not phosphorylated in infected cells. The RNase L activity associated with 2',5'-oligoadenylate synthetase is not activated or is blocked, since cellular RNA is not degraded. These results are consistent with lack of protein translation shutoff early following infection. We used a well-established recombinant vaccinia virus (VV)-based expression system that lacks the viral IFN antagonist E3L to screen viral genes for their ability to rescue the IFN sensitivity of the mutant. The nucleocapsid (N) gene rescued VV{Delta}E3L from IFN sensitivity. N gene expression prevents cellular RNA degradation and partially rescues the dramatic translation shutoff characteristic of the VV{Delta}E3L virus. However, it does not prevent PKR phosphorylation. The results indicate that the MHV N protein is a type I IFN antagonist that likely plays a role in circumventing the innate immune response.

* Corresponding author. Mailing address: The Biodesign Institute, P.O. Box 875401, Arizona State University, Tempe, AZ 85287-5401. Phone: (480) 965-9478. Fax: (480) 727-7615. E-mail: Brenda.Hogue{at}asu.edu.

{triangledown} Published ahead of print on 20 December 2006.

{dagger} Y.Y. and K.H. contributed equally to this work.

Journal of Virology, March 2007, p. 2554-2563, Vol. 81, No. 6
0022-538X/07/$08.00+0     doi:10.1128/JVI.01634-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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