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¹ Laboratory of Viral Immunobiology, ² Christopher H. Browne Center for Immunology and Immune Diseases, ³ Laboratory of Virology and Infectious Disease, and ⁴ Center for the Study of Hepatitis C, The Rockefeller University, New York, NY 10065
⁵ Department of Pathology, Weill-Cornell Medical College, New York Presbyterian Hospital, New York, NY 10065
⁶ Medical Virology Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
⁷ Department of Pediatrics and ⁸ Laboratory of Cellular Immunobiology and Adult Allogeneic Bone Marrow Transplantation Service, Division of Hematologic Oncology, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10065
⁹ Inflammatory Effector Mechanisms Laboratory, Hospital for Special Surgery, New York, NY 10021
¹⁰ Viral Immunobiology, Institute of Experimental Immunology, University Hospital Zürich, 8091 Zürich, Switzerland

CORRESPONDENCE Christian Münz: christian.muenz{at}usz.ch

Many pathogens that cause human disease infect only humans. To identify the mechanisms of immune protection against these pathogens and also to evaluate promising vaccine candidates, a small animal model would be desirable. We demonstrate that primary T cell responses in mice with reconstituted human immune system components control infection with the oncogenic and persistent Epstein-Barr virus (EBV). These cytotoxic and interferon-–producing T cell responses were human leukocyte antigen (HLA) restricted and specific for EBV-derived peptides. In HLA-A2 transgenic animals and similar to human EBV carriers, T cell responses against lytic EBV antigens dominated over recognition of latent EBV antigens. T cell depletion resulted in elevated viral loads and emergence of EBV-associated lymphoproliferative disease. Both loss of CD4⁺ and CD8⁺ T cells abolished immune control. Therefore, this mouse model recapitulates features of symptomatic primary EBV infection and generates T cell–mediated immune control that resists oncogenic transformation.

Abbreviations used: EBER, EBV-encoded RNA; EBNA, nuclear antigen of EBV; HPC, hematopoietic progenitor cell; IM, infectious mononucleosis; LCL, lymphoblastoid cell line; LMP, latent membrane protein; RIU, Raji-infecting units.

© 2009 Strowig et al.
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