This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Greene, I. P.
Right arrow Articles by Weaver, S. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Greene, I. P.
Right arrow Articles by Weaver, S. C.

 Previous Article  |  Next Article 

Journal of Virology, July 2005, p. 9128-9133, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.9128-9133.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Envelope Glycoprotein Mutations Mediate Equine Amplification and Virulence of Epizootic Venezuelan Equine Encephalitis Virus

Ivorlyne P. Greene,1,2 Slobodan Paessler,1,2 Laura Austgen,3 Michael Anishchenko,1,2 Aaron C. Brault,1,2,{dagger} Richard A. Bowen,3 and Scott C. Weaver1,2*

Center for Biodefense and Emerging Infectious Diseases,1 Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555-0609,2 Animal Reproduction and Biotechnology Lab, Colorado State University, Ft. Collins, Colorado 805223

Received 14 February 2004/ Accepted 26 March 2005

Epidemics of Venezuelan equine encephalitis (VEE) result from high-titer equine viremia of IAB and IC subtype viruses that mediate increased mosquito transmission and spillover to humans. Previous genetic studies suggest that mutations in the E2 envelope glycoprotein allow relatively viremia-incompetent, enzootic subtype ID strains to adapt for equine replication, leading to VEE emergence. To test this hypothesis directly, chimeric VEEV strains containing the genetic backbone of enzootic subtype ID strains and the partial envelope glycoprotein genes of epizootic subtype IC and IAB strains, as well as reciprocal chimeras, were used for experimental infections of horses. Insertion of envelope genes from two different, closely related enzootic subtype ID strains into the epizootic backbones resulted in attenuation, demonstrating that the epizootic envelope genes are necessary for the equine-virulent and viremia-competent phenotypes. The partial epizootic envelope genes introduced into an enzootic ID backbone were sufficient to generate the virulent, viremia-competent equine phenotype. These results indicate that a small number of envelope gene mutations can generate an equine amplification-competent, epizootic VEEV from an enzootic progenitor and underscore the limitations of small animal models for evaluating and predicting the epizootic phenotype.

* 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.

{dagger} Present address: Center for Vector-borne Diseases and Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616.

Journal of Virology, July 2005, p. 9128-9133, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.9128-9133.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Konopka, J. L., Thompson, J. M., Whitmore, A. C., Webb, D. L., Johnston, R. E. (2009). Acute Infection with Venezuelan Equine Encephalitis Virus Replicon Particles Catalyzes a Systemic Antiviral State and Protects from Lethal Virus Challenge. J. Virol. 83: 12432-12442 [Abstract] [Full Text]  
  • Simmons, J. D., White, L. J., Morrison, T. E., Montgomery, S. A., Whitmore, A. C., Johnston, R. E., Heise, M. T. (2009). Venezuelan Equine Encephalitis Virus Disrupts STAT1 Signaling by Distinct Mechanisms Independent of Host Shutoff. J. Virol. 83: 10571-10581 [Abstract] [Full Text]  
  • Aguilar, P. V., Adams, A. P., Wang, E., Kang, W., Carrara, A.-S., Anishchenko, M., Frolov, I., Weaver, S. C. (2008). Structural and Nonstructural Protein Genome Regions of Eastern Equine Encephalitis Virus Are Determinants of Interferon Sensitivity and Murine Virulence. J. Virol. 82: 4920-4930 [Abstract] [Full Text]  
  • Coffey, L. L., Vasilakis, N., Brault, A. C., Powers, A. M., Tripet, F., Weaver, S. C. (2008). Arbovirus evolution in vivo is constrained by host alternation. Proc. Natl. Acad. Sci. USA 105: 6970-6975 [Abstract] [Full Text]  
  • Powers, A. M., Logue, C. H. (2007). Changing patterns of chikungunya virus: re-emergence of a zoonotic arbovirus. J. Gen. Virol. 88: 2363-2377 [Full Text]  
  • Wang, E., Paessler, S., Aguilar, P. V., Carrara, A.-S., Ni, H., Greene, I. P., Weaver, S. C. (2006). Reverse Transcription-PCR-Enzyme-Linked Immunosorbent Assay for Rapid Detection and Differentiation of Alphavirus Infections. J. Clin. Microbiol. 44: 4000-4008 [Abstract] [Full Text]  
  • Anishchenko, M., Bowen, R. A., Paessler, S., Austgen, L., Greene, I. P., Weaver, S. C. (2006). From the Cover: Venezuelan encephalitis emergence mediated by a phylogenetically predicted viral mutation. Proc. Natl. Acad. Sci. USA 103: 4994-4999 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»