The S2 accessory gene of equine infectious anemia virus is essential for expression of disease in ponies

Equine infectious anemia virus (EIAV) is a macrophage-tropic lentivirus that persistently infects horses and causes a disease that is characterized by periodic episodes of fever, thrombocytopenia, and viremia. EIAV encodes only four regulatory/accessory genes, ( tat, rev, ttm, and S2) and is the lea...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2006-05, Vol.349 (1), p.22-30
Main Authors: Fagerness, Angela J., Flaherty, Maureen T., Perry, Stephanie T., Jia, Bin, Payne, Susan L., Fuller, Frederick J.
Format: Article
Language:English
Subjects:
Accessory gene deletion
Amino Acid Sequence
Animals
Blood - virology
Body Temperature
Cell Line
Dogs
Equine Infectious Anemia - physiopathology
Equine Infectious Anemia - virology
Equine infectious anemia virus
Gene Deletion
Genes, Essential
Genes, Viral
Horses
Infectious Anemia Virus, Equine - genetics
Infectious Anemia Virus, Equine - pathogenicity
Lentivirus
Macrophages - virology
Mutagenesis, Site-Directed
Pathogenesis mutant
RNA-Directed DNA Polymerase - analysis
S2 accessory gene
Sequence Homology
Viral Load
Viral pathogenesis
Viral Proteins - genetics
Viral Proteins - physiology
Virus Replication
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Summary:Equine infectious anemia virus (EIAV) is a macrophage-tropic lentivirus that persistently infects horses and causes a disease that is characterized by periodic episodes of fever, thrombocytopenia, and viremia. EIAV encodes only four regulatory/accessory genes, ( tat, rev, ttm, and S2) and is the least genetically complex of all known lentiviruses. We sought to determine the role of the EIAV S2 accessory gene of EIAV by introducing mutations that would prevent S2 expression on the p19/wenv17 infectious molecular clone. Virus derived from the p19/wenv17 molecular clone is highly virulent and routinely fatal when given in high doses (J. Virol. 72 (1998) 483). In contrast, an S2 deletion mutant on the p19/wenv17 background is unable to induce acute disease and plasma virus loads were reduced by 2.5 to 4.0 logs at 15 days post-infection. The S2 deleted virus failed to produce any detectable clinical signs during a 5-month observation period. These results demonstrate that S2 gene expression is essential for disease expression of EIAV.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2005.12.041