Journal of Virology, April 2001, p. 4008-4013, Vol. 75, No. 8
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.8.4008-4013.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Molecular Medicine Unit, St. James's University Hospital, University of Leeds, Leeds LS9 7TF, United Kingdom,1 and Institut für Klinische und Molekulare Virologie der Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054 Erlangen, Germany2
Received 6 November 2000/Accepted 15 January 2001
Herpesviruses occur in two distinct forms of infection, lytic replication and latent persistence. In this study, we investigated the molecular mechanisms that govern the latent-lytic switch in the prototype gamma-2 herpesvirus, herpesvirus saimiri (HVS). We utilized a persistently HVS-infected A549 cell line, in which HVS DNA is stably maintained as nonintegrated circular episomes, to assess the role of the open reading frame 50 (ORF 50) (Rta) proteins in the latent-lytic switch. Northern blot analysis and virus recovery assays determined that the ORF 50a gene product, when expressed under the control of a constitutively active promoter, was sufficient to reactivate the entire lytic replication cycle, producing infectious virus particles. Furthermore, although the ORF 50 proteins of HVS strains A11 and C488 are structurally divergent, they were both capable of inducing the lytic replication cycle in this model of HVS latency.
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