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Epizootic strains of Venezuelan equine encephalitis virus (VEEV) cause epidemics by exploiting equines as highly efficient amplification hosts for mosquito transmission. Although phylogenetic studies indicate that epizootic VEEV strains emerge via mutation from enzootic progenitors that are incapable of efficient equine amplification, the molecular mechanism(s) involved remain enigmatic. The convergent evolution of E2 envelope glycoprotein mutations suggests that they are critical to VEEV emergence, but little is known about the role of non-envelope genes. We used the guinea pig, the small animal model that best predicts the ability to generate equine viremia, to assess the role of envelope versus other mutations in the epizootic phenotype. Using reciprocal chimeric viruses generated by swapping the envelope genes of closely related epizootic IC and enzootic ID strains, infections of guinea pigs demonstrated that envelope and non-envelope genes and sequences both contributed to virulence. However, early replication in lymphoid tissues appeared to be primarily envelope dependent.
Received August 25, 2004. Accepted for publication October 3, 2004.
Acknowledgments: We thank Amelia Travassos da Rosa for technical assistance and John Roehrig (Centers for Disease Control and Prevention, Fort Collins, CO) for providing monoclonal antibodies.
Financial support: Ivorlyne P. Greene was supported by National Institutes of Health (NIH) minority supplemental grant AI-10984, Ivorlyne P. Greene and Darci R. Smith were supported by the Centers for Disease Control and Prevention Vector-Borne Infectious Disease Training Program 417760. Slobodan Paessler was supported by the NIH Emerging and Tropical Diseases T32 Training grant AI-107536. Aaron C. Brault was supported by the James L. McLaughlin Fellowship Fund and the NIH Emerging and Tropical Diseases T32 Training grant AI-107526. This research was supported by NIH grants AI-39800 and AI-48807.
Authors’ addresses: Ivorlyne P. Greene, Johns Hopkins University, School of Public Health, Department of Molecular Microbiology and Immunology, 615 N. Wolfe St., WS114, Baltimore, MD 21205; Slobodan Paessler, Michael Anishchenko, and Darci R. Smith, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555-0609. Aaron C. Brault, Department of Pathology, Microbiology and Immunology, Center for Vector-Borne Diseases, School of Veterinary Medicine, University of California, Davis, CA 95616. Ilya Frolov, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-0609. Scott C. Weaver, Center for Biodefense and Emerging Infectious Diseases, Department of Pathology, and Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-0609, Telephone : 409-747-0758, Fax : 409-747-2415, E-mail : sweaver{at}utmb.edu.
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