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Nonsegmented Negative-Sense RNA Viruses Utilize N6-Methyladenosine (m6A) as a Common Strategy To Evade Host Innate

Mijia Lu1, Miaoge Xue1, Hai-Tao Wang2,3

  • 1Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio, USA.

Journal of Virology
|February 4, 2021
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Summary

Many viruses use N6-Methyladenosine (m6A) RNA methylation to evade host immunity. Removing m6A from viral RNA boosts innate immune responses, suggesting a new vaccine development strategy.

Keywords:
N6-methyladenosineinnate immunitynegative-strand RNA virus

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • N6-Methyladenosine (m6A) is a crucial RNA modification.
  • Viruses often incorporate m6A into their RNA, but its function is unclear.
  • Host innate immunity distinguishes self from non-self RNA.

Purpose of the Study:

  • Investigate the role of viral m6A methylation in host innate immune evasion.
  • Determine if m6A methylation is a conserved mechanism among nonsegmented negative-sense (NNS) RNA viruses.
  • Explore potential therapeutic strategies targeting viral RNA modifications.

Main Methods:

  • Utilized m6A methyltransferase (METTL3) knockout cells to generate m6A-deficient viral RNAs.
  • Assessed type I interferon responses in relation to viral RNA m6A status.
  • Analyzed RIG-I pathway activation, including RIG-I binding, ubiquitination, and oligomerization.
  • Investigated the role of YTHDF2 in regulating interferon signaling.

Main Results:

  • m6A-deficient viral RNAs from Pneumoviridae, Paramyxoviridae, and Rhabdoviridae families triggered higher type I interferon responses.
  • The RIG-I pathway mediated the increased interferon response to m6A-deficient viral RNA.
  • m6A-deficient viral RNA showed enhanced RIG-I interaction and pathway activation.
  • YTHDF2 was found to be essential for suppressing type I interferon signaling.

Conclusions:

  • Viral m6A methylation is a conserved strategy for NNS RNA viruses to evade host innate immunity.
  • The absence of m6A on viral RNA enhances recognition by the RIG-I innate immune pathway.
  • Targeting viral RNA m6A modification could be a novel approach for vaccine development to boost innate immunity.