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Home / Equine Research Bank / J Virol / cis- and trans-acting regulation of gene expression of equin...
Journal of virology1988; 62(9); 3522-3526; doi: 10.1128/JVI.62.9.3522-3526.1988

cis- and trans-acting regulation of gene expression of equine infectious anemia virus.

Abstract: Deletion analysis of the equine infectious anemia virus long terminal repeat revealed that sequences responsive to virus-specific transactivation are located within the region spanning the transcriptional start site (-31 to +22). In addition, an active exon of a trans-acting factor (tat) was identified downstream of pol and overlapping env (nucleotides 5264 to 5461). Activation by tat is accompanied by an increase in the steady-state levels of mRNA directed by the equine infectious anemia virus long terminal repeat.
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Publication Date: 1988-09-01 PubMed ID: 2841502PubMed Central: PMC253482DOI: 10.1128/JVI.62.9.3522-3526.1988Google 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 discusses the gene expression of equine infectious anemia virus, focusing on how certain sequences in the virus’s long terminal repeat and a certain downstream factor (tat) impact the virus’s transactivation.

Overall Context of the Research

  • The investigation targeted the gene expression mechanisms of equine infectious anemia virus (EIAV). The primary interest was to understand the role of specific genetic sequences in virus transactivation.
  • Transactivation refers to the process where one region of a genetic sequence influences the activity of a separate sequence. In this context, it involves how different parts of the EIAV’s genetic makeup affect each other to facilitate the virus’s operations, such as replication and infection.
  • In the context of viruses, long terminal repeats (LTRs) are significant regulatory sequences found at both ends of the virus’s genome. They play key roles in virus replication and integration into the host genome.

Identifying cis- and trans-Acting Factors

  • The researchers carried out a deletion analysis on the EIAV’s long terminal repeat (LTR), helping them identify the sequences responsible for virus-specific transactivation.
  • The researchers found that these sequences span the transcriptional start site, which is the section of DNA where transcription begins.
  • The study also identified an active exon of a trans-acting factor named ‘tat’ downstream of pol and overlapping env in the EIAV genome. The ‘tat’ gene plays an essential role in increasing the production of viral proteins, boosting virus replication.

Functional Implications of Findings

  • Activation by ‘tat’ leads to an increase in the steady-state levels of mRNA directed by the equine infectious anemia virus long terminal repeat (LTR). This process is likely to enhance the virus’s ability to produce proteins and, consequently, its infectivity and propagation.
  • Recognising the essential role of these genes can offer avenues for developing therapeutic interventions against the EIAV. Targeting these genes could potentially hinder the virus’s replication process, thereby diminishing its potency.
  • Understanding the role of these specific sequences in virus transactivation also helps broaden general virology knowledge, potentially offering insights that could apply to other viruses in addition to the equine infectious anemia virus.

Cite This Article

APA
Dorn PL, Derse D. (1988). cis- and trans-acting regulation of gene expression of equine infectious anemia virus. J Virol, 62(9), 3522-3526. https://doi.org/10.1128/JVI.62.9.3522-3526.1988

Publication

Journal of virology
ISSN: 0022-538X
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 62
Issue: 9
Pages: 3522-3526

Researcher Affiliations

Dorn, P L
  • Biological Carcinogenesis Development Program, National Cancer Institute Frederick Cancer Research Facility, Maryland 21701-1013.
Derse, D

    MeSH Terms

    • Animals
    • Cell Line
    • Exons
    • Gene Expression Regulation
    • Gene Products, tat
    • Infectious Anemia Virus, Equine / genetics
    • Plasmids
    • RNA, Viral / biosynthesis
    • Repetitive Sequences, Nucleic Acid
    • Transcription Factors / genetics
    • Transcription, Genetic
    • Transfection

    Grant Funding

    • N01-CO-74102 / NCI NIH HHS

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