期刊
BLOOD
卷 104, 期 5, 页码 1482-1489出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2004-01-0342
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- NCI NIH HHS [CA 65319, CA 68051] Funding Source: Medline
- NCRR NIH HHS [P51 RR 00168] Funding Source: Medline
- NIDCR NIH HHS [DE 14388Q] Funding Source: Medline
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 10(8) 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. (C) 2004 by The American Society of Hematology.
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