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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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NEOPLASIA

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

From the Departments of Medicine and Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; and the Departments of Primate Resources, Immunology, and Pathology, New England Primate Research Center, Harvard Medical School, Southborough, MA.

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 4 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 4 additional immunosuppressed animals. Two animals with modest immunosuppression remained asymptomatic, and 1 of 2 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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