Aug 17, 2004

Generation of a latency-deficient gammaherpesvirus that is protective against secondary infection

Journal of Virology
Tammy M RickabaughRen Sun

Abstract

Kaposi's sarcoma-associated herpesvirus and murine gammaherpesvirus-68 (MHV-68) establish latent infections and are associated with various types of malignancies. They are members of the gamma-2 herpesvirus subfamily and encode a replication and transcriptional activator, RTA, which is necessary and sufficient to disrupt latency and initiate the viral lytic cycle in vitro. We have constructed a recombinant MHV-68 virus that overexpresses RTA. This virus has faster replication kinetics in vitro and in vivo, is deficient in establishing latency, exhibits a reduction in the development of a mononucleosis-like disease in mice, and can protect mice against challenge by wild-type MHV-68. The present study, by using MHV-68 as an in vivo model system, demonstrated that RTA plays a critical role in the control of viral latency and suggests that latency is a determinant of viral pathogenesis in vivo.

Mentioned in this Paper

Human herpesvirus 8
Infectious Mononucleosis
Superinfection
Immediate-Early Proteins
Latent Virus Infection Process
Mice, Inbred BALB C
Lung
Lytic Phase
Simplexvirus
Viral Proteins

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