The S2 accessory gene of equine infectious anemia virus is essential for expression of disease in ponies.
Abstract: 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.
Publication Date: 2006-02-28 PubMed ID: 16503341DOI: 10.1016/j.virol.2005.12.041Google Scholar: Lookup
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- Journal Article
- Research Support
- N.I.H.
- Extramural
Summary
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This study focuses on understanding the role of the S2 accessory gene in the Equine infectious anemia virus (EIAV), a virus that affects horses and is characterized by periodic episodes of fever, thrombocytopenia, and viremia. The researchers discovered that a mutation preventing the expression of S2 makes the virus unable to induce acute disease in horses, suggesting that the S2 gene is crucial for disease manifestation.
The Equine Infectious Anemia Virus (EIAV)
- EIAV is a macrophage-tropic lentivirus infecting horses and causes a disease characterized by periodic episodes of fever, thrombocytopenia, and viremia.
- The virus encodes only four regulatory/accessory genes: tat, rev, ttm, and S2, making it the least genetically complex of all known lentiviruses.
- The p19/wenv17 molecular clone of EIAV is particularly virulent and often proves fatal when administered in high doses.
The Role of the S2 Accessory Gene
- The research study specifically focused on understanding the role of the S2 accessory gene within EIAV.
- This was achieved by introducing mutations that prevent the expression of the S2 gene in the p19/wenv17 infectious molecular clone.
- The mutation essentially nullified the virulence of EIAV: the S2-deleted virus could not induce acute disease, and plasma virus loads were significantly reduced (by 2.5 to 4.0 logs) 15 days post-infection.
- The S2-deleted virus also failed to produce any detectable clinical signs in the afflicted horses over a 5-month observation period.
Implications of the Research
- The research findings have crucial implications for understanding the pathology of EIAV and potentially other similar viruses.
- It has been unequivocally proven that the S2 gene expression is essential for disease expression of EIAV.
- This opens up potential avenues for the development of targeted treatments by manipulating the S2 gene, either for disease prevention or management.
Cite This Article
APA
Fagerness AJ, Flaherty MT, Perry ST, Jia B, Payne SL, Fuller FJ.
(2006).
The S2 accessory gene of equine infectious anemia virus is essential for expression of disease in ponies.
Virology, 349(1), 22-30.
https://doi.org/10.1016/j.virol.2005.12.041 Publication
Researcher Affiliations
- Department of Public Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606-8401, USA. ahfagern@ksu.edu
MeSH Terms
- Amino Acid Sequence
- Animals
- Blood / virology
- Body Temperature
- Cell Line
- Dogs
- Equine Infectious Anemia / physiopathology
- Equine Infectious Anemia / virology
- Gene Deletion
- Genes, Essential
- Genes, Viral
- Horses
- Infectious Anemia Virus, Equine / genetics
- Infectious Anemia Virus, Equine / pathogenicity
- Macrophages / virology
- Mutagenesis, Site-Directed
- RNA-Directed DNA Polymerase / analysis
- Sequence Homology
- Viral Load
- Viral Proteins / genetics
- Viral Proteins / physiology
- Virus Replication
Grant Funding
- CA-59278 / NCI NIH HHS
Citations
This article has been cited 13 times.- Wang XF, Zhang X, Ma W, Li J, Wang X. Host cell restriction factors of equine infectious anemia virus.. Virol Sin 2023 Aug;38(4):485-496.
- Munis AM. Gene Therapy Applications of Non-Human Lentiviral Vectors.. Viruses 2020 Sep 29;12(10).
- Ahmad I, Li S, Li R, Chai Q, Zhang L, Wang B, Yu C, Zheng YH. The retroviral accessory proteins S2, Nef, and glycoMA use similar mechanisms for antagonizing the host restriction factor SERINC5.. J Biol Chem 2019 Apr 26;294(17):7013-7024.
- Cavalieri V, Baiamonte E, Lo Iacono M. Non-Primate Lentiviral Vectors and Their Applications in Gene Therapy for Ocular Disorders.. Viruses 2018 Jun 9;10(6).
- Gonzalez-Enriquez GV, Escoto-Delgadillo M, Vazquez-Valls E, Torres-Mendoza BM. SERINC as a Restriction Factor to Inhibit Viral Infectivity and the Interaction with HIV.. J Immunol Res 2017;2017:1548905.
- Ahi YS, Zhang S, Thappeta Y, Denman A, Feizpour A, Gummuluru S, Reinhard B, Muriaux D, Fivash MJ, Rein A. Functional Interplay Between Murine Leukemia Virus Glycogag, Serinc5, and Surface Glycoprotein Governs Virus Entry, with Opposite Effects on Gammaretroviral and Ebolavirus Glycoproteins.. mBio 2016 Nov 22;7(6).
- Chande A, Cuccurullo EC, Rosa A, Ziglio S, Carpenter S, Pizzato M. S2 from equine infectious anemia virus is an infectivity factor which counteracts the retroviral inhibitors SERINC5 and SERINC3.. Proc Natl Acad Sci U S A 2016 Nov 15;113(46):13197-13202.
- Choi J, Ryoo J, Oh C, Hwang S, Ahn K. SAMHD1 specifically restricts retroviruses through its RNase activity.. Retrovirology 2015 Jun 2;12:46.
- Wang XF, Wang S, Liu Q, Lin YZ, Du C, Tang YD, Na L, Wang X, Zhou JH. A unique evolution of the s2 gene of equine infectious anemia virus in hosts correlated with particular infection statuses.. Viruses 2014 Nov 10;6(11):4265-79.
- Yin X, Hu Z, Gu Q, Wu X, Zheng YH, Wei P, Wang X. Equine tetherin blocks retrovirus release and its activity is antagonized by equine infectious anemia virus envelope protein.. J Virol 2014 Jan;88(2):1259-70.
- Covaleda L, Gno BT, Fuller FJ, Payne SL. Identification of cellular proteins interacting with equine infectious anemia virus S2 protein.. Virus Res 2010 Aug;151(2):235-9.
- Covaleda L, Fuller FJ, Payne SL. EIAV S2 enhances pro-inflammatory cytokine and chemokine response in infected macrophages.. Virology 2010 Feb 5;397(1):217-23.
- Zielonka J, Bravo IG, Marino D, Conrad E, Perković M, Battenberg M, Cichutek K, Münk C. Restriction of equine infectious anemia virus by equine APOBEC3 cytidine deaminases.. J Virol 2009 Aug;83(15):7547-59.
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