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Superantigen-Activated T Cells Redirected by a Bispecific Antibody Inhibit Vesicular Stomatitis Virus Replication In Vitro and In Vivo¹

Ana Fernandez-Sesma^*, Richard W. Peluso, Xu Bai, Jerome L. Schulman^*, David E. Levy^§ and Thomas M. Moran^2,*

^* Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029; Quality Biotech, Division of Virology, Camdem, NJ 08104; Department of Immunobiology, Mount Sinai School of Medicine, New York, NY 10029; and ^§ Department of Pathology and Kaplan Cancer Center, New York University School of Medicine, New York, NY 10016

A bispecific Ab (BsAb) that binds the TCR on T cells and the G protein of the vesicular stomatitis virus (VSV) can redirect staphylococcal enterotoxin B (SEB)-activated T cells to kill VSV-infected cells and to inhibit VSV replication in vitro. Inhibition of virus replication in our system is dependent upon the specificity of the Ab for the viral protein. IFN- does not play a very important role in this phenomenon, which is mainly mediated by the release of Pfp from CD8⁺ T cells. We have used a Stat1 knockout mouse model in which VSV infection is lethal. Infusion of staphylococcal enterotoxin-activated B T cells and bispecific Ab significantly slowed virus progression and prolonged the survival of VSV-infected Stat1 knockout mice in vivo.