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Blood, 1 September 2004, Vol. 104, No. 5, pp. 1482-1489.
Prepublished online as a Blood First Edition Paper on May 18, 2004; DOI 10.1182/blood-2004-01-0342.
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Submitted January 28, 2004
Accepted April 29, 2004
Experimental Rhesus Lymphocryptovirus Infection in Immunosuppressed Macaques: An Animal Model for Epstein-Barr Virus Pathogenesis in the Immunosuppressed Host
Pierre Rivailler, Angela Carville, Amitinder Kaur, Pasupuleti Rao, Carol Quink, Jeffery L Kutok, Susan Westmoreland, Sherry Klumpp, Meredith Simon, Jon C Aster, and Fred Wang*
Medicine, Brigham & Women's Hospital, Boston, MA, USA
Primate Resources, New England Primate Research Center, Southborough, MA, USA
Immunology, New England Primate Research Center, Southborough, MA, USA
Pathology, Brigham & Women's Hospital, Boston, MA, USA
Pathology, New England Primate Research Center, Southborough, MA, USA
* Corresponding author; email: fwang{at}rics.bwh.harvard.edu.
To develop a model for Epstein-Barr virus (EBV) pathogenesis in immunosuppressed hosts, we studied experimental infections of immunocompetent versus SHIV 89.6P infected, immunosuppressed rhesus macaques with the EBV-related rhesus lymphocryptovirus (LCV). Primary LCV infection after oral inoculation of four immunocompetent animals was characterized by an acute viremia and seroconversion followed by asymptomatic LCV persistence. Four immunosuppressed macaques infected orally with LCV failed to develop an LCV-specific humoral response and viremia was more pronounced, but there was no evidence of LCV-induced lymphoproliferative disease. A more aggressive primary challenge was administered by intravenous inoculation of 108 autologous, LCV-immortalized B cells in four additional immunosuppressed animals. Two animals with modest immunosuppression remained asymptomatic, and one of two severely immunosuppressed animals developed an aggressive, monoclonal LCV-positive lymphoma. These studies demonstrate the potential for lymphomagenesis in an experimental model system for EBV infection and underscore the strength and depth of immune control in limiting LCV-induced lymphoproliferative disease.
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