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Home / Equine Research Bank / J Virol / Equine infectious anemia virus Gag p9 function in early step...
Journal of virology2005; 79(14); 8793-8801; doi: 10.1128/JVI.79.14.8793-8801.2005

Equine infectious anemia virus Gag p9 function in early steps of virus infection and provirus production.

Abstract: We have previously reported that serial truncation of the Gag p9 protein of equine infectious anemia virus (EIAV) revealed a progressive loss in replication phenotypes in transfected cells, such that a proviral mutant (E32) expressing the N-terminal 31 amino acids of p9 produced infectious virus particles similarly to parental provirus, while a proviral mutant (K30) with two fewer amino acids produced replication-defective virus particles, despite containing apparently normal levels of processed Gag and Pol proteins (C. Chen, F. Li, and R. C. Montelaro, J. Virol. 75:9762-9760, 2001). Based on these observations, we sought in the current study to identify the precise defect in K30 virion infection of permissive equine dermal (ED) cells. The results of these experiments clearly demonstrated that K30 virions entered target ED cells and produced early (minus-strand strong-stop) and late (Gag) viral DNA products as efficiently as did the replication-competent E32 mutant and parental EIAV(UK) viruses. However, in contrast to the replication-competent E32 mutant and parental viruses, infection with K30 mutant virus failed to produce detectable two-long-terminal-repeat DNA circles, stable integrated provirus, virus-specific Gag mRNA expression, or intracellular viral protein expression. Taken together, these data demonstrate that the K30 mutant is defective in the ability to produce sufficient nuclear viral DNA to establish a productive infection in ED cells. Thus, these observations indicate for the first time that the EIAV Gag p9 protein performs a critical role in viral DNA production and processing to provirus during EIAV infection, in addition to its previously defined role in viral budding mediated by the p9 L domain.
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Publication Date: 2005-07-05 PubMed ID: 15994773PubMed Central: PMC1168773DOI: 10.1128/JVI.79.14.8793-8801.2005Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research article focuses on the function of the Gag p9 protein of the equine infectious anemia virus (EIAV), particularly in the early stages of virus infection and provirus production. The researchers discovered that a specific strain of the virus (K30) is unable to effectively produce nuclear viral DNA, thereby inhibiting its ability to establish a productive infection in equine dermal cells.

Objective

The study centered on understanding how the truncation and absence of certain amino acids in the EIAV Gag p9 protein impacted the virus’ ability to infect cells and reproduce. Key results showed that a specific proviral mutant (K30) failed to produce two-long-terminal-repeat DNA circles and stably integrate its provirus.

Methodology

  • The researchers made use of serial truncation of the EIAV Gag p9 protein, creating mutant strains with varying lengths of this protein.
  • They conducted their study with two proviral mutants— E32 and K30, each having different lengths of the p9 protein.
  • The infection and replication ability of these mutants were observed in experiments on equine dermal cells.

Results

  • The research found that the K30 mutant entered the target cells and created early and late viral DNA products as effectively as the E32 mutant and the parental EIAV.
  • However, unlike the latter, the K30 strain couldn’t produce the necessary DNA circles or establish a significant provirus, thereby inhibiting the expression of virus-specific Gag mRNA and intracellular viral protein.
  • These findings led to the conclusion that the K30 mutant lacked the ability to generate enough nuclear viral DNA to cause a productive infection in equine dermal cells.

Significance

  • The study offers key insights into the role of the EIAV Gag p9 protein in the virus’ lifecycle, suggesting it plays a critical role in viral DNA production, processing to provirus during EIAV infection, in addition to its previously defined role in viral budding.
  • This understanding can prove beneficial in the development of treatments against EIAV, as the disruption of the Gag p9 protein could potentially halt the spread of the virus within hosts.

Cite This Article

APA
Jin S, Chen C, Montelaro RC. (2005). Equine infectious anemia virus Gag p9 function in early steps of virus infection and provirus production. J Virol, 79(14), 8793-8801. https://doi.org/10.1128/JVI.79.14.8793-8801.2005

Publication

Journal of virology
ISSN: 0022-538X
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 79
Issue: 14
Pages: 8793-8801

Researcher Affiliations

Jin, Sha
  • Department of Molecular Genetics and Biochemistry, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Chen, Chaoping
    Montelaro, Ronald C

      MeSH Terms

      • Active Transport, Cell Nucleus
      • Animals
      • COS Cells
      • DNA, Viral / biosynthesis
      • Gene Products, gag / physiology
      • Horses
      • Infectious Anemia Virus, Equine / physiology
      • Proviruses / physiology
      • Transcription, Genetic
      • Viral Proteins / biosynthesis
      • Virus Integration
      • Virus Replication

      Grant Funding

      • R01 CA049296 / NCI NIH HHS
      • R01 CA49296 / NCI NIH HHS

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