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Journal of Virology, September 2005, p. 11300-11310, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.11300-11310.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Variation in Interferon Sensitivity and Induction among Strains of Eastern Equine Encephalitis Virus

Patricia V. Aguilar,1,2 Slobodan Paessler,1,3 Anne-Sophie Carrara,1,3 Samuel Baron,2 Joyce Poast,2 Eryu Wang,1,3 Abelardo C. Moncayo,1,3 Michael Anishchenko,1,3 Douglas Watts,1,3 Robert B. Tesh,1,3 and Scott C. Weaver1,2,3*

Center for Biodefense and Emerging Infectious Diseases,1 Department of Microbiology and Immunology,2 Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555-06093

Received 2 November 2004/ Accepted 10 May 2005

Eastern equine encephalitis virus (EEEV) causes human encephalitis in North America (NA), but in South America (SA) it has rarely been associated with human disease, suggesting that SA strains are less virulent. To evaluate the hypothesis that this virulence difference is due to a greater ability of NA strains to evade innate immunity, we compared replication of NA and SA strains in Vero cells pretreated with interferon (IFN). Human IFN-{alpha}, -ß, and -{gamma} generally exhibited less effect on replication of NA than SA strains, supporting this hypothesis. In the murine model, no consistent difference in IFN induction was observed between NA and SA strains. After infection with most EEEV strains, higher viremia levels and shorter survival times were observed in mice deficient in IFN-{alpha}/ß receptors than in wild-type mice, suggesting that IFN-{alpha}/ß is important in controlling replication. In contrast, IFN-{gamma} receptor-deficient mice infected with NA and SA strains had similar viremia levels and mortality rates to those of wild-type mice, suggesting that IFN-{gamma} does not play a major role in murine protection. Mice pretreated with poly(I-C), a nonspecific IFN inducer, exhibited dose-dependent protection against fatal eastern equine encephalitis, further evidence that IFN is important in controlling disease. Overall, our in vivo results did not support the hypothesis that NA strains are more virulent in humans due to their greater ability to counteract the IFN response. However, further studies using a better model of human disease are needed to confirm the results of differential human IFN sensitivity obtained in our in vitro experiments.

* Corresponding author. Mailing address: Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555-0609. Phone: (409) 747-0758. Fax: (409) 747-2415. E-mail: sweaver{at}utmb.edu.

Journal of Virology, September 2005, p. 11300-11310, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.11300-11310.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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