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Journal of Virology, July 2005, p. 8707-8715, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.8707-8715.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Human Cytomegalovirus TRS1 and IRS1 Gene Products Block the Double-Stranded-RNA-Activated Host Protein Shutoff Response Induced by Herpes Simplex Virus Type 1 Infection

Kevin A. Cassady*

Department of Pediatrics, the University of Alabama at Birmingham, Birmingham, Alabama, 35233

Received 26 January 2005/ Accepted 21 March 2005

Human cytomegalovirus (HCMV) attachment and entry stimulates the expression of cellular interferon-inducible genes, many of which target important cellular functions necessary for viral replication. Double-stranded RNA-dependent host protein kinase (PKR) is an interferon-inducible gene product that limits viral replication by inhibiting protein translation in the infected cell. It was anticipated that HCMV encodes gene products that facilitate the evasion of this PKR-mediated antiviral response. Using a {Delta}{gamma}134.5 herpes simplex virus type 1 (HSV-1) recombinant that triggers PKR-mediated protein synthesis shutoff, experiments identified an HCMV gene product expressed in the initial hours of infection that allows continued protein synthesis in the infected cell. Recombinant HSV-1 viruses expressing either the HCMV TRS1 or IRS1 protein demonstrate that either of these HCMV gene products allows the {Delta}{gamma}134.5 recombinant viruses to evade PKR-mediated protein shutoff and maintain late viral protein synthesis.

* Mailing address: UAB Department of Pediatrics, 1600 6th Avenue South, CHB-118C, Birmingham, AL 35233. Phone: (205) 996-7876. Fax: (205) 975-1992. E-mail: kcassady{at}peds.uab.edu.

Journal of Virology, July 2005, p. 8707-8715, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.8707-8715.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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