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Journal of Virology, October 2006, p. 9381-9390, Vol. 80, No. 19
0022-538X/06/$08.00+0     doi:10.1128/JVI.01061-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

ICP22 Is Required for Wild-Type Composition and Infectivity of Herpes Simplex Virus Type 1 Virions

Joseph S. Orlando,1,2 John W. Balliet,1,2 Anna S. Kushnir,1,2 Todd L. Astor,3 Magdalena Kosz-Vnenchak,4 Stephen A. Rice,5 David M. Knipe,1 and Priscilla A. Schaffer1,2*

Departments of Microbiology and Molecular Genetics, Harvard Medical School,1 Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215,2 Department of Clinical Pediatrics, The Ohio State University, Columbus, Ohio 43205,3 Laboratory of Molecular Genetics and Virology, Jagiellonian University Medical College, Cracow, Poland,4 Department of Microbiology, University of Minnesota Medical School, Minneapolis, Minnesota 554555

Received 23 May 2006/ Accepted 6 July 2006

The immediate-early regulatory protein ICP22 is required for efficient replication of herpes simplex virus type 1 in some cell types (permissive) but not in others (restrictive). In mice infected via the ocular route, the pathogenesis of an ICP22– virus, 22/n199, was altered relative to that of wild-type virus. Specifically, tear film titers of 22/n199-infected mice were significantly reduced at 3 h postinfection relative to those of mice infected with wild-type virus. Further, 22/n199 virus titers were below the level of detection in trigeminal ganglia (TG) during the first 9 days postinfection. On day 30 postinfection, TG from 22/n199-infected mice contained reduced viral genome loads and exhibited reduced expression of latency-associated transcripts and reduced reactivation efficiency relative to TG from wild-type virus-infected mice. Notably, the first detectable alteration in the pathogenesis of 22/n199 in these tests occurred in the eye prior to the onset of nascent virus production. Thus, ICP22– virions appeared to be degraded, cleared, or adsorbed more rapidly than wild-type virions, implying potential differences in the composition of the two virion types. Analysis of the protein composition of purified extracellular virions indicated that ICP22 is not a virion component and that 22/n199 virions sediment at a reduced density relative to wild-type virions. Although similar to wild-type virions morphologically, 22/n199 virions contain reduced amounts of two {gamma}2 late proteins, US11 and gC, and increased amounts of two immediate-early proteins, ICP0 and ICP4, as well as protein species not detected in wild-type virions. Although ICP22– viruses replicate to near-wild-type levels in permissive cells, the virions produced in these cells are biochemically and physically different from wild-type virions. These virion-specific differences in ICP22– viruses add a new level of complexity to the functional analysis of this immediate-early viral regulatory protein.

* Corresponding author. Mailing address: Department of Medicine, Harvard Medical School at the Beth Israel Deaconess Medical Center, 330 Brookline Avenue, RN 123, Boston, MA 02215. Phone: (617) 667-2958. Fax: (617) 667-8540. E-mail: pschaffe{at}bidmc.harvard.edu.

Journal of Virology, October 2006, p. 9381-9390, Vol. 80, No. 19
0022-538X/06/$08.00+0     doi:10.1128/JVI.01061-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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