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Journal of Virology, November 2007, p. 12535-12542, Vol. 81, No. 22
0022-538X/07/$08.00+0     doi:10.1128/JVI.00197-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

A Recombinant Sendai Virus Is Controlled by CD4+ Effector T Cells Responding to a Secreted Human Immunodeficiency Virus Type 1 Envelope Glycoprotein{triangledown}

Scott A. Brown,1,2* Julia L. Hurwitz,1,2,3 Amy Zirkel,2 Sherri Surman,1,2 Toru Takimoto,2,5 Irina Alymova,2 Chris Coleclough,1,3,7 Allen Portner,2,3 Peter C. Doherty,1,6 and Karen S. Slobod1,4

Departments of Immunology,1 Infectious Diseases, St. Jude Children's Research Hospital, 332 N. Lauderdale, Memphis, Tennessee,2 Departments of Pathology,3 Pediatrics, University of Tennessee, Memphis, Tennessee,4 Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 672, Rochester, New York 14642,5 Department of Microbiology and Immunology, University of Melbourne, Victoria 3010, Australia,6 Silver Bullet Biology, Memphis, Tennessee7

Received 29 January 2007/ Accepted 19 June 2007

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 human immunodeficiency virus type 1 (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 gamma interferon, and interleukin-2 (IL-2), IL-4, and IL-5 in that site, and (iii) significantly reduced pulmonary viral load. The challenge experiments were repeated with immunoglobulin–/– 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 further dissecting CD4+ T-cell-mediated immunity in the lung.

* Corresponding author. Mailing address: Department of Immunology, 332 N. Lauderdale, Memphis, TN 38105. Phone: (901) 495-2650. Fax: (901) 495-3099. E-mail: address:scott.brown{at}stjude.org

{triangledown} Published ahead of print on 25 July 2007.

Journal of Virology, November 2007, p. 12535-12542, Vol. 81, No. 22
0022-538X/07/$08.00+0     doi:10.1128/JVI.00197-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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