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J Virol, August 1998, p. 6770-6776, Vol. 72, No. 8
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
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
orf14) was constructed with a deletion in the orf14 gene. The
transforming potential of HVS
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
orf14 mutant did not produce such a growth transformation. In addition, HVS
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
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.
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