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Journal of Virology, January 2004, p. 1-8, Vol. 78, No. 1
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.1.1-8.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Generation and Characterization of Closely Related Epizootic and Enzootic Infectious cDNA Clones for Studying Interferon Sensitivity and Emergence Mechanisms of Venezuelan Equine Encephalitis Virus

Michael Anishchenko,1,2 Slobodan Paessler,1,2 Ivorlyne P. Greene,1,2 Patricia V. Aguilar,1,3 Anne-Sophie Carrara,1,2 and Scott C. Weaver1,2,3*

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

Received 13 June 2003/ Accepted 30 September 2003

Venezuelan equine encephalitis virus (VEEV) is a reemerging pathogen and a continuing threat to humans and equines in the Americas. Identification of the genetic determinants that enable epizootic VEEV strains to arise and exploit equines as amplification hosts to cause widespread human disease is pivotal to understanding VEE emergence. The sensitivity to murine alpha/beta interferon-mediated antiviral activity was previously correlated to the epizootic phenotype of several VEEV strains. Infectious cDNA clones were generated from an epizootic subtype IC VEEV strain (SH3) isolated during the 1992 Venezuelan outbreak and a closely related enzootic, sympatric subtype ID strain (ZPC738). These VEEV strains had low-cell-culture-passage histories and differed by only 12 amino acids in the nonstructural and structural proteins. Rescued viruses showed similar growth kinetics to their parent viruses in several cell lines, and murine infections resulted in comparable viremia and disease. Unlike what was found in other studies of epizootic and enzootic VEEV strains, the sensitivities to murine alpha/beta interferon did not differ appreciably between these epizootic versus enzootic strains, calling into question the reliability of interferon sensitivity as a marker of epizootic potential.

* Corresponding author. Mailing address: Department of Pathology, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-0609. Phone: (409) 747-0758. Fax: (409) 747-2415. E-mail: sweaver{at}utmb.edu.

Journal of Virology, January 2004, p. 1-8, Vol. 78, No. 1
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.1.1-8.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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