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Virology2016; 495; 112-121; doi: 10.1016/j.virol.2016.04.024

Equine schlafen 11 restricts the production of equine infectious anemia virus via a codon usage-dependent mechanism.

Abstract: Human schlafen11 is a novel restriction factor for HIV-1 based on bias regarding relative synonymous codon usage (RSCU). Here, we report the cloning of equine schlafen11 (eSLFN11) and the characteristics of its role in restricting the production of equine infectious anemia virus (EIAV), a retrovirus similar to HIV-1. Overexpression of eSLFN11 inhibited EIAV replication, whereas knockdown of endogenous eSLFN11 by siRNA enhanced the release of EIAV from its principal target cell. Notably, although eSLFN11 significantly suppressed expression of viral Gag protein and EIAV release into the culture medium, the levels of intracellular viral early gene proteins Tat and Rev and viral genomic RNA were unaffected. Coincidently, similar altered patterns of codon usage bias were observed for both the early and late genes of EIAV. Therefore, our data suggest that eSLFN11 restricts EIAV production by impairing viral mRNA translation via a mechanism that is similar to that employed by hSLFN11 for HIV-1.
Copyright © 2016 Elsevier Inc. All rights reserved.
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Publication Date: 2016-05-18 PubMed ID: 27200480DOI: 10.1016/j.virol.2016.04.024Google Scholar: Lookup
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  • Research Support
  • Non-U.S. Gov't

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 explores how equine schlafen11, a horse-based gene, can hamper the replication of equine infectious anemia virus, an HIV-1-like virus.

Overview of Research

In this study, scientists cloned the gene equine schlafen11, also known as eSLFN11, to understand its role in fighting off the equine infectious anemia virus (EIAV). The research draws parallels to the human equivalent of the gene, human schlafen11 (hSLFN11), which is known to obstruct the HIV-1 virus.

Key Findings and Methodology

  • The researchers found that increasing the presence of eSLFN11 within a cell led to the restriction of EIAV replication.
  • Inversely, when the eSLFN11 gene was suppressed via siRNA, a type of molecule known to silence gene expression, the release of EIAV from its target cell was notably enhanced.
  • The effect of eSLFN11, however, didn’t influence the early stage viral proteins, Tat and Rev, and the viral genomic RNA, indicating that its restriction mechanism is specific to certain parts of the virus’s life cycle.

Significance of the Codon Usage Pattern

  • The researchers observed specific patterns of codon usage bias, a phenomenon where specific codons (sequences of three DNA or RNA nucleotides) are favored over others, in both early and late genes of EIAV.
  • This observation led the researchers to propose that eSLFN11 hinders EIAV by impairing the translation of viral mRNA, a process that creates proteins using genes’ instructions.
  • The manner in which eSLFN11 impedes EIAV production is likened to the way hSLFN11 restricts HIV-1, lending further credence to the theory that these genes could be utilized therapeutically in future treatments.

Implications and Future Research

  • The findings in this study may lead to the development of new antiviral therapies that exploit SLFN11 or other similar genes’ virus restriction capabilities.
  • Further research is needed to fully understand the mechanism of eSLFN11 and how it can be optimized for maximum viral restriction. Additionally, other potential genes with similar properties could also be investigated.

Cite This Article

APA
Lin YZ, Sun LK, Zhu DT, Hu Z, Wang XF, Du C, Wang YH, Wang XJ, Zhou JH. (2016). Equine schlafen 11 restricts the production of equine infectious anemia virus via a codon usage-dependent mechanism. Virology, 495, 112-121. https://doi.org/10.1016/j.virol.2016.04.024

Publication

Virology
ISSN: 1096-0341
NlmUniqueID: 0110674
Country: United States
Language: English
Volume: 495
Pages: 112-121

Researcher Affiliations

Lin, Yue-Zhi
  • Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Science, Harbin, China. Electronic address: sndhr@163.com.
Sun, Liu-Ke
  • Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Science, Harbin, China. Electronic address: sunlk0916@126.com.
Zhu, Dan-Tong
  • Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Science, Harbin, China; College of Wildlife Resources, Northeast Forestry University, Harbin, China. Electronic address: zhudantong123@163.com.
Hu, Zhe
  • Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Science, Harbin, China. Electronic address: huzher@126.com.
Wang, Xue-Feng
  • Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Science, Harbin, China. Electronic address: xuefengwang1982@126.com.
Du, Cheng
  • Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Science, Harbin, China. Electronic address: chengdᦁ@163.com.
Wang, Yu-Hong
  • Department of Geriatrics And Gerontology, First Affiliated Hospital of Harbin Medical University, Harbin, China. Electronic address: wang_yu_hong@163.com.
Wang, Xiao-Jun
  • Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Science, Harbin, China. Electronic address: xjw@hvri.ac.cn.
Zhou, Jian-Hua
  • Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Science, Harbin, China. Electronic address: jianhua_uc@126.com.

MeSH Terms

  • Amino Acid Sequence
  • Animals
  • Codon
  • Gene Expression Regulation, Viral
  • Gene Knockdown Techniques
  • Genome, Viral
  • HIV-1 / physiology
  • Horses
  • Humans
  • Infectious Anemia Virus, Equine / physiology
  • Nuclear Proteins / chemistry
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism
  • RNA, Small Interfering / genetics
  • RNA, Viral
  • Transcription, Genetic
  • Viral Proteins / chemistry
  • Viral Proteins / genetics
  • Viral Proteins / metabolism
  • Virus Release
  • Virus Replication

Citations

This article has been cited 23 times.
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