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Journal of Virology, April 2005, p. 5059-5068, Vol. 79, No. 8
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.8.5059-5068.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Susanna Colaco, and
Philip G. Stevenson*
Division of Virology, Department of Pathology, University of Cambridge, Cambridge, United Kingdom
Received 23 November 2004/ Accepted 16 January 2005
Herpesviruses remain predominantly cell associated within their hosts, implying that they spread between cells by a mechanism distinct from free virion release. We previously identified the efficient release of murine gammaherpesvirus 68 (MHV-68) virions as a function of the viral gp150 protein. Here we show that the MHV-68 ORF27 gene product, gp48, contributes to the direct spread of viruses from lytically infected to uninfected cells. Monoclonal antibodies to gp48 identified it on infected cell surfaces and in virions. gp48-deficient viruses showed no obvious deficit in virion cell binding, single-cycle replication, or virion release but had reduced lytic propagation between cells. After intranasal infection of mice, ORF27-deficient viruses were impaired predominantly in lytic replication in the lungs. There was a small deficit in latency establishment, but long-term latency appeared normal. Since ORF27 has homologs in both Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus, it is likely part of a conserved mechanism employed by gammaherpesviruses to disseminate lytically in their hosts.
Present address: Cambridge Institute for Medical Research, University of Cambridge School of Clinical Medicine, Cambridge CB2 2XY, United Kingdom.
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