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J Virol, August 1998, p. 6770-6776, Vol. 72, No. 8
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

A Role for Herpesvirus Saimiri orf14 in Transformation and Persistent Infection

Monroe Duboise,1,2 Jie Guo,1 Sue Czajak,1 Heuiran Lee,1 Ronald Veazey,3 Ronald C. Desrosiers,1 and Jae U. Jung1,*

Department of Microbiology and Molecular Genetics1 and Department of Pathology,3 New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772-9102, and Department of Applied Medical Sciences, University of Southern Maine, Portland, Maine 04104-93002

Received 4 March 1998/Accepted 14 May 1998

The product of open reading frame 14 (orf14) of herpesvirus saimiri (HVS) exhibits significant homology with mouse mammary tumor virus superantigen. orf14 encodes a 50-kDa secreted glycoprotein, as shown previously (Z. Yao, E. Maraskovsky, M. K. Spriggs, J. I. Cohen, R. J. Armitage, and M. R. Alderson, J. Immunol. 156:3260-3266, 1996). orf14 expressed from recombinant baculovirus powerfully induces proliferation of CD4-positive cells originating from several different species. To study the role of orf14 in transformation, a mutant form of HVS (HVS Delta orf14) was constructed with a deletion in the orf14 gene. The transforming potential of HVS Delta orf14 was tested in cell culture and in common marmosets. Parental HVS subgroup C strain 488 immortalized common marmoset T lymphocytes in vitro to interleukin-2-independent growth, while the HVS Delta orf14 mutant did not produce such a growth transformation. In addition, HVS Delta orf14 was nononcogenic in common marmosets. In contrast to other nononcogenic HVS mutant viruses which were repeatedly isolated from peripheral blood mononuclear cells of infected marmosets for more than 5 months, HVS Delta orf14 did not persist at a high level in vivo. These results demonstrate that orf14 of HVS is not required for replication but is required for transformation and for high-level persistence in vivo.

* Corresponding author. Mailing address: New England Regional Primate Research Center, Harvard Medical School, P.O. Box 9102, Southborough, MA 01772-9102. Phone: (508) 624-8083. Fax: (508) 624-8190. E-mail: jjung{at}warren.med.harvard.edu.

J Virol, August 1998, p. 6770-6776, Vol. 72, No. 8
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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