Respiratory Syncytial Virus Utilizes a tRNA Fragment to Suppress Antiviral Responses Through a Novel Targeting Mechanism

Junfang Deng, Ryan N. Ptashkin, Yu Chen, Zhi Cheng, Guangliang Liu, Thien Phan, Xiaoling Deng, Jiehua Zhou, Inhan Lee, Yong Sun Lee, Xiaoyong Bao

Research output: Contribution to journalArticlepeer-review

50 Scopus citations

Abstract

Target identification is highly instructive in defining the biological roles of microRNAs. However, little is known about other small noncoding RNAs; for example, tRNA-derived RNA Fragments (tRFs). Some tRFs exhibit a gene-silencing mechanism distinctly different from that of typical microRNAs. We recently demonstrated that a respiratory syncytial virus (RSV)-induced tRF, called tRF5-GluCTC, promotes RSV replication. RSV is the single most important cause of lower respiratory tract infection in children. By using biochemical screening and bioinformatics analyses, we have identified apolipoprotein E receptor 2 (APOER2) as a target of tRF5-GluCTC. The 3′-portion of tRF5-GluCTC recognizes a target site in the 3′-untranslated region of APOER2 and suppresses its expression. We have also discovered that APOER2 is an anti-RSV protein whose suppression by tRF5-GluCTC promotes RSV replication. Our report represents the first identification of a natural target of a tRF and illustrates how a virus utilizes a host tRF to control a host gene to favor its replication.

Original languageEnglish (US)
Pages (from-to)1622-1629
Number of pages8
JournalMolecular Therapy
Volume23
Issue number10
DOIs
StatePublished - Oct 1 2015

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Pharmacology
  • Drug Discovery

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