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

 Previous Article  |  Next Article 

J. Virol., Jan 1998, 483-487, Vol 72, No. 1
Copyright © 1998, American Society for Microbiology

Disease induction by virus derived from molecular clones of equine infectious anemia virus

SL Payne, XM Qi, H Shao, A Dwyer and FJ Fuller
Department of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-4960, USA. spayne@utarlg.uta.edu

Equine infectious anemia virus (EIAV), a macrophage-tropic lentivirus, causes persistent infections of horses. A number of biologic features, including the rapid development of acute disease, the episodic nature of chronic disease, the propensity for viral genetic variation, and the ability for many infected animals to eventually control virus replication, render EIAV a potentially useful model system for the testing of antiretroviral therapies and vaccine strategies. The utility of the EIAV system has been hampered by the lack of proviral clones that encode promptly pathogenic viral stocks. In this report, we describe the generation and characterization of two infectious molecular clones capable of causing acute clinical syndromes similar to those seen in natural infections. Virus derived from clone p19/wenv17 caused severe debilitating disease at 5 to 7 days postinfection; initial febrile episodes were fatal in two of three infected animals. Virus derived from a second clone, p19/wenv16, caused somewhat milder primary febrile episodes by 10 to 12 days postinfection in two of two infected animals. Virus derived from both clones caused persistent infections such that some animals exhibited chronic equine infectious anemia, characterized by multiple disease episodes. The two virulent clones differ in envelope and rev sequences.

This article has been cited by other articles:

• Payne, S. L., Pei, X.-f., Jia, B., Fagerness, A., Fuller, F. J. (2004). Influence of Long Terminal Repeat and Env on the Virulence Phenotype of Equine Infectious Anemia Virus. J. Virol. 78: 2478-2485 [Abstract] [Full Text]  
• Maury, W., Wright, P. J., Bradley, S. (2003). Characterization of a Cytolytic Strain of Equine Infectious Anemia Virus. J. Virol. 77: 2385-2399 [Abstract] [Full Text]  
• Payne, S., La Celle, K, Pei, X., Qi, X., Shao, H, Steagall, W., Perry, S, Fuller, F (1999). Long terminal repeat sequences of equine infectious anaemia virus are a major determinant of cell tropism. J. Gen. Virol. 80: 755-759 [Abstract]