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J. Virol. doi:10.1128/JVI.00197-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

A recombinant Sendai virus is controlled by CD4+ effector T cells responding to a secreted HIV-1 envelope glycoprotein

Departments of, Immunology and; Infectious Diseases, St. Jude Children's Research Hospital, 332 N. Lauderdale, Memphis, TN, Departments of, Pathology and; Pediatrics, University of Tennessee, Memphis, TN, and Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 672, Rochester, NY 14642, USA, Department of Microbiology and Immunology, University of Melbourne, Victoria 3010, Australia

^* To whom correspondence should be addressed. Email: scott.brown{at}stjude.org.

	Abstract

The importance of antigen-specific CD4+ helper T cells in virus infections is well recognized, but their possible role as direct mediators of virus clearance is less well characterized. Here we describe a recombinant Sendai virus strategy for probing the effector role(s) of CD4+ T cells. Mice were vaccinated with DNA and vaccinia virus recombinant vectors encoding a secreted HIV-1-envelope protein, and then challenged with a Sendai virus carrying a homologous HIV-1 envelope gene. The primed mice showed (i) prompt homing of numerous envelope-primed CD4+ T cell populations to the virus-infected lung, (ii) substantial production of IFN-, IL-2, IL-4 and IL-5 in that site, and (iii) significantly reduced pulmonary viral load. The challenge experiments were repeated in Ig^-/- µMT mice, in the presence or absence of CD8+ and/or CD4+ T cells. These selectively immunodeficient mice were protected by primed CD4+ T cells, in the absence of antibody or CD8+ T cells. Together, these results highlight the role of CD4+ T cells as direct effectors in vivo and, because this protocol gives such a potent response, identify an outstanding experimental model for the further dissection of CD4⁺ T cell-mediated immunity in the lung.