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Journal of Virology, September 2007, p. 9870-9877, Vol. 81, No. 18
0022-538X/07/$08.00+0 doi:10.1128/JVI.00001-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Division of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 136-713,1 Department of Microbiology, College of Medicine, Hallym University, Chuncheon 200-702, Republic of Korea,2 Department of Molecular and Medical Pharmacology, University of California at Los Angeles, Los Angeles, California 900953
Received 2 January 2007/ Accepted 28 June 2007
Our functional mapping study of murine gammaherpesvirus 68 (MHV-68, or
HV-68) revealed that a mutant harboring a transposon at the ORF49 locus (ORF49null) evidenced a highly attenuated in vitro growth. ORF49 resides adjacent to and in an opposite direction from RTA, the primary switch of the gammaherpesvirus life cycle. A FLAG-tagged ORF49 protein was able to transcomplement ORF49null, and a revertant of ORF49null restored its attenuated growth to a level comparable to that of the wild type. The FLAG-tagged ORF49 protein promoted the ability of RTA to activate downstream target promoters and enhanced virus replication from the ORF50null virus in the presence of RTA. Furthermore, ORF49 enhanced wild-type virus replication by increasing the RTA transcript levels. Our data indicate that ORF49 may perform an important function in MHV-68 replication in cooperation with RTA.
Published ahead of print on 18 July 2007.
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