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Journal of Virology, September 2002, p. 9398-9406, Vol. 76, No. 18
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.18.9398-9406.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

The Antiviral Efficacy of the Murine Alpha-1 Interferon Transgene against Ocular Herpes Simplex Virus Type 1 Requires the Presence of CD4+, {alpha}/ß T-Cell Receptor-Positive T Lymphocytes with the Capacity To Produce Gamma Interferon

Daniel J. J. Carr1,2* and Sansanee Noisakran1

Departments of Ophthalmology,1 Microbiology and Immunology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 731042

Received 11 March 2002/ Accepted 20 June 2002

Alpha/beta interferons (IFN-{alpha}/ßs) are known to antagonize herpes simplex virus type 1 (HSV-1) infection by directly blocking viral replication and promoting additional innate and adaptive, antiviral immune responses. To further define the relationship between the adaptive immune response and IFN-{alpha}/ß, the protective effect induced following the topical application of plasmid DNA containing the murine IFN-{alpha}1 transgene onto the corneas of wild-type and T-cell-deficient mice was evaluated. Mice homozygous for both the T-cell receptor (TCR) ß- and {delta}-targeted mutations expressing no {alpha}ß or {gamma}{delta} TCR ({alpha}ß/{gamma}{delta} TCR double knockout [dKO]) treated with the IFN-{alpha}1 transgene succumbed to ocular HSV-1 infection at a rate similar to that of {alpha}ß/{gamma}{delta} TCR dKO mice treated with the plasmid vector DNA. Conversely, mice with targeted disruption of the TCR {delta} chain and expressing no {gamma}{delta} TCR+ cells treated with the IFN-{alpha}1 transgene survived the infection to a greater extent than the plasmid vector-treated counterpart and at a level similar to that of wild-type controls treated with the IFN-{alpha}1 transgene. By comparison, mice with targeted disruption of the TCR ß chain and expressing no {alpha}ß TCR+ cells ({alpha}ß TCR knockout [KO]) showed no difference upon treatment with the IFN-{alpha}1 transgene or the plasmid vector control, with 0% survival following HSV-1 infection. Adoptively transferring CD4+ but not CD8+ T cells from wild-type but not IFN-{gamma}-deficient mice reestablished the antiviral efficacy of the IFN-{alpha}1 transgene in {alpha}ß TCR KO mice. Collectively, the results indicate that the protective effect mediated by topical application of a plasmid construct containing the murine IFN-{alpha}1 transgene requires the presence of CD4+ T cells capable of IFN-{gamma} synthesis.

* Corresponding author. Mailing address: Department of Ophthalmology, DMEI #415, OUHSC, 608 Stanton L. Young Blvd., Oklahoma City, OK 73104. Phone: (405) 271-1084. Fax: (405) 271-8781. E-mail: dan-carr{at}ouhsc.edu.

Journal of Virology, September 2002, p. 9398-9406, Vol. 76, No. 18
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.18.9398-9406.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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