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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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