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Current HIV research2010; 8(1); 66-72; doi: 10.2174/157016210790416352

Virulence determinants of equine infectious anemia virus.

Abstract: Equine infectious anemia virus (EIAV) is a macrophage-tropic lentivirus that rapidly Induces disease in experimentally infected horses. Because EIAV infection and replication is centered on the monocyte/macrophage and has a pronounced acute disease stage, it is a useful model system for understanding the contribution of monocyte/macrophages to other lentivirus-induced diseases. Genetic mapping studies utilizing chimeric proviruses in which parental viruses are acutely virulent or avirulent have allowed the identification of important regions that influence acute virulence. U3 regions in the viral LTR, surface envelope (SU) protein and the accessory S2 gene strongly influence acute disease expression. While the chimeric proviruses provide insight into genes or genome regions that affect viral pathogenesis, it is then necessary to further dissect those regions to focus on specific virus-host mechanisms that lead to disease expression. The V6 region of the viral env protein is an example of one identified region that may interact with the ELR-1 receptor in an important way and we are currently identifying S2 protein motifs required for disease expression.
Publication Date: 2010-03-10 PubMed ID: 20210781DOI: 10.2174/157016210790416352Google Scholar: Lookup
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Summary

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This research focuses on understanding how Equine Infectious Anemia Virus (EIAV), a virus causing disease in horses, operates at a genetic level and identifies key regions that influence the severity of the disease.

Understanding EIAV

  • The research revolves around Equine Infectious Anemia Virus (EIAV), a type of lentivirus that targets monocytes/macrophages causing a severe instant disease in horses. The investigation provides insight into the role of monocytes/macrophages in lentivirus-induced diseases.

Genetic Mapping and Chimeric Proviruses

  • The study employed genetic mapping using chimeric proviruses. The approach allows for the creation of hybrid viruses by combining genetic material from virulent (disease-causing) and avirulent (not causing disease) viruses.
  • The findings help researchers identify critical regions influencing the intensity of the acute (instant or severe) virulence of the virus.

Key Viral Regions Impacting Disease Expression

  • The study revealed that the U3 regions in the viral Long Terminal Repeat (LTR), the Surface Envelope (SU) protein, and the supplementary S2 gene significantly influence the acute expression of the disease.
  • Discovering these regions provides an understanding of crucial areas affecting the virus’s ability to cause illness, crucial for exploring targeted treatments or prevention strategies.

Identifying Virus-Host Interaction Mechanisms

  • While identifying key areas of the viral genome important to pathogenicity, it is necessary to further investigate these regions to determine specific virus-host interaction mechanisms leading to disease expression.
  • An example given in the research is the V6 region of the viral env protein, which may interact significantly with the ELR-1 receptor.
  • The researchers are also looking into identifying the S2 protein patterns essential for triggering disease expression.

Cite This Article

APA
Payne SL, Fuller FJ. (2010). Virulence determinants of equine infectious anemia virus. Curr HIV Res, 8(1), 66-72. https://doi.org/10.2174/157016210790416352

Publication

ISSN: 1873-4251
NlmUniqueID: 101156990
Country: Netherlands
Language: English
Volume: 8
Issue: 1
Pages: 66-72

Researcher Affiliations

Payne, Susan L
  • Department of Pathobiology, College of Veterinary Medicine, Texas A & M University, 4467 TAMU, College Station, TX 77843-4467, USA. spayne@cvm.tamu.edu
Fuller, Frederick J

    MeSH Terms

    • Animals
    • Disease Models, Animal
    • Equine Infectious Anemia / virology
    • Horses
    • Host-Pathogen Interactions
    • Infectious Anemia Virus, Equine / genetics
    • Infectious Anemia Virus, Equine / pathogenicity
    • Macrophages
    • Terminal Repeat Sequences
    • Viral Tropism
    • Virulence Factors
    • Virus Replication

    Citations

    This article has been cited 6 times.
    1. Kemeter LM, Birzer A, Heym S, Thoma-Kress AK. Milk Transmission of Mammalian Retroviruses.. Microorganisms 2023 Jul 8;11(7).
    2. Wang HN, Rao D, Fu XQ, Hu MM, Dong JG. Equine infectious anemia virus in China.. Oncotarget 2018 Jan 2;9(1):1356-1364.
      doi: 10.18632/oncotarget.20381pubmed: 29416700google scholar: lookup
    3. Wang XF, Liu Q, Wang YH, Wang S, Chen J, Lin YZ, Ma J, Zhou JH, Wang X. Characterization of Equine Infectious Anemia Virus Long Terminal Repeat Quasispecies In Vitro and In Vivo.. J Virol 2018 Apr 15;92(8).
      doi: 10.1128/JVI.02150-17pubmed: 29386282google scholar: lookup
    4. Cervantes DT, Ball JM, Edwards J, Payne S. Horses naturally infected with EIAV harbor 2 distinct SU populations but are monophyletic with respect to IN.. Virus Genes 2016 Feb;52(1):71-80.
      doi: 10.1007/s11262-015-1280-zpubmed: 26739458google scholar: lookup
    5. 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.
      doi: 10.3390/v6114265pubmed: 25390683google scholar: lookup
    6. Qi X, Wang X, Wang S, Lin Y, Jiang C, Ma J, Zhao L, Lv X, Shen R, Wang F, Kong X, Su Z, Zhou J. Genomic analysis of an effective lentiviral vaccine-attenuated equine infectious anemia virus vaccine EIAV FDDV13.. Virus Genes 2010 Aug;41(1):86-98.
      doi: 10.1007/s11262-010-0491-6pubmed: 20526660google scholar: lookup