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Journal of Virology, September 1999, p. 7381-7389, Vol. 73, No. 9
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Inhibition of Antigen Presentation by the
Glycine/Alanine Repeat Domain Is Not Conserved in Simian Homologues of
Epstein-Barr Virus Nuclear Antigen 1
Neil W.
Blake,1
Amir
Moghaddam,2
Pasupuleti
Rao,2
Amitinder
Kaur,3
Rhona
Glickman,3
Young-gyu
Cho,2
Andrew
Marchini,4
Tracey
Haigh,1
R. Paul
Johnson,3,5
Alan B.
Rickinson,1 and
Fred
Wang2,*
CRC Institute for Cancer Studies, University
of Birmingham Medical School, Edgbaston, Birmingham B15 2TA, United
Kingdom1; Department of Immunology, New
England Regional Primate Research Center, Harvard Medical School,
Southborough, Massachusetts 017723;
Partners AIDS Research Center and Infectious Disease Unit,
Massachusetts General Hospital,5 and
Department of Medicine, Brigham and Women's
Hospital,2 Harvard Medical School, Boston,
Massachusetts 02115; and Howard Hughes Medical Institute,
Princeton University, Princeton, New Jersey 085444
Received 11 May 1999/Accepted 1 June 1999
Most humans and Old World nonhuman primates are infected for life
with Epstein-Barr virus (EBV) or closely related gammaherpesviruses in
the same lymphocryptovirus (LCV) subgroup. Several potential strategies
for immune evasion and persistence have been proposed based on studies
of EBV infection in humans, but it has been difficult to test their
actual contribution experimentally. Interest has focused on the EBV
nuclear antigen 1 (EBNA1) because of its essential role in the
maintenance and replication of the episomal viral genome in latently
infected cells and because EBNA1 endogenously expressed in these cells
is protected from presentation to the major histocompatibility complex
class-I restricted cytotoxic T-lymphocyte (CTL) response through the
action of an internal glycine-alanine repeat (GAR). Given the high
degree of biologic conservation among LCVs which infect humans and Old
World primates, we hypothesized that strategies essential for viral
persistence would be well conserved among viruses of this subgroup. We
show that the rhesus LCV EBNA1 shares sequence homology with the EBV and baboon LCV EBNA1 and that the rhesus LCV EBNA1 is a functional homologue for EBV EBNA1-dependent plasmid maintenance and replication. Interestingly, all three LCVs possess a GAR domain, but the baboon and
rhesus LCV EBNA1 GARs fail to inhibit antigen processing and presentation as determined by using three different in vitro CTL assays. These studies suggest that inhibition of antigen processing and
presentation by the EBNA1 GAR may not be an essential mechanism for
persistent infection by all LCV and that other mechanisms may be
important for immune evasion during LCV infection.
*
Corresponding author. Mailing address: Channing
Laboratories, 181 Longwood Ave., Boston, MA 02115. Phone: (617)
525-4258. Fax: (617) 525-4257. E-mail:
fwang{at}rics.bwh.harvard.edu.
Journal of Virology, September 1999, p. 7381-7389, Vol. 73, No. 9
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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