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Journal of Virology, July 2000, p. 6680-6683, Vol. 74, No. 14
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Gamma Interferon Impedes the Establishment of Herpes Simplex Virus Type 1 Latent Infection but Has No Impact on Its Maintenance or Reactivation in Mice

Julie A. Lekstrom-Himes, Rona A. LeBlanc, Lesley Pesnicak, Matthew Godleski, and Stephen E. Straus*

Medical Virology Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland

Received 20 August 1999/Accepted 14 April 2000

Murine models of gamma interferon (IFN-gamma ) deficiency demonstrate the role of this cytokine in attenuating acute herpes simplex virus (HSV) disease; however, the effect of IFN-gamma on the establishment and maintenance of neuronal latency and viral reactivation is not known. Using the IFN-gamma knockout (GKO) model of IFN-gamma deficiency and sensitive quantitative PCR methods, we show that IFN-gamma significantly reduces the ganglion content of latent HSV-1 in BALB/c mice, which in turn delays viral time to reactivation following UV irradiation. Similar effects were not seen in the C57BL/6 strain. These results indicate that IFN-gamma significantly attenuates latent HSV infection in the mouse model of ocular infection but has no impact on the maintenance of latency or virus reactivation.

* Corresponding author. Mailing address: 10 Center Dr., 11N228, Bethesda, MD 20892. Phone: (301) 496-5807. Fax: (301) 496-7383. E-mail: sstraus{at}nih.gov.

Journal of Virology, July 2000, p. 6680-6683, Vol. 74, No. 14
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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