Evidence map›Paper›PMID 32753500›Full record

ArticlemBio2020

Mechanism and Function of Antiviral RNA Interference in Mice.

Qingxia Han, Gang Chen, Jinyan Wang, David Jee, Wan-Xiang Li, Eric C Lai, Shou-Wei Ding

Open access · goldAbstract read
In one paragraph

Article in mBio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Infection Defects of RNA and DNA Viruses Induced by Antiviral RNA Interference.Microbiology and molecular biology reviews : MMBR · 2023
    Review
  8. Article
  9. Potential of siRNA in COVID-19 therapy: Emphasis onFrontiers in bioengineering and biotechnology · 2023
    Review
  10. Mammalian viral suppressors of RNA interference.Trends in biochemical sciences · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. HYL1-CLEAVAGE SUBTILASE 1 (HCS1) suppresses miRNA biogenesis in response to light-to-dark transition.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Qingxia Han *Department of Microbiology and Plant Pathology, University of California, Riverside, Riverside, California, USA.
Gang Chen *Department of Microbiology and Plant Pathology, University of California, Riverside, Riverside, California, USA.
Jinyan WangDepartment of Microbiology and Plant Pathology, University of California, Riverside, Riverside, California, USA.
David JeeDepartment of Developmental Biology, Sloan Kettering Institute, New York, New York, USA.
Wan-Xiang LiDepartment of Microbiology and Plant Pathology, University of California, Riverside, Riverside, California, USA.
Eric C LaiDepartment of Developmental Biology, Sloan Kettering Institute, New York, New York, USA.
Shou-Wei DingDepartment of Microbiology and Plant Pathology, University of California, Riverside, Riverside, California, USA shou-wei.ding@ucr.edu.
University of California, Riverside · USKettering University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Selective regulatory and biogenesis mechanisms for microRNAsR01GM083300 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI Eric C Lai · 2007 to 2026
$9.8M
Gene Silencing as an Antiviral Defense in Animal CellsR01AI052447 · NIAID · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI DING, SHOU-WEI · 2003 to 2016
$6.0M
Molecular and genetic analysis of novel Slicer-dependent miRNA pathways in bloodR01HL135564 · NHLBI · SLOAN-KETTERING INST CAN RESEARCH · PI KHARAS, MICHAEL, LAI, ERIC C · 2017 to 2020
$2.9M
Function and mechanism of the mammalian RNA interference response to virus infectionR01AI141887 · NIAID · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI DING, SHOU-WEI · 2019 to 2022
$2.3M
Antiviral immunity directed by virus-derived small silencing RNAs in miceR56AI110579 · NIAID · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI DING, SHOU-WEI · 2015 to 2015
$372k
NCI NIH HHS P30 CA008748NHLBI NIH HHS R01 HL135564NIAID NIH HHS R01 AI052447NIAID NIH HHS R01 AI141887NIAID NIH HHS R56 AI110579NIGMS NIH HHS R01 GM083300
6 · The paper itself

Abstract

Distinct mammalian RNA viruses trigger Dicer-mediated production of virus-derived small-interfering RNAs (vsiRNA) and encode unrelated proteins to suppress vsiRNA biogenesis. However, the mechanism and function of the mammalian RNA interference (RNAi) response are poorly understood. Here, we characterized antiviral RNAi in a mouse model of infection with Nodamura virus (NoV), a mosquito-transmissible positive-strand RNA virus encoding a known double-stranded RNA (dsRNA)-binding viral suppressor of RNAi (VSR), the B2 protein. We show that inhibition of NoV RNA replication by antiviral RNAi in mouse embryonic fibroblasts (MEFs) requires Dicer-dependent vsiRNA biogenesis and Argonaute-2 slicer activity. We found that VSR-B2 of NoV enhances viral RNA replication in wild-type but not RNAi-defective MEFs such as Argonaute-2 catalytic-dead MEFs and Dicer or Argonaute-2 knockout MEFs, indicating that VSR-B2 acts mainly by suppressing antiviral RNAi in the differentiated murine cells. Consistently, VSR-B2 expression in MEFs has no detectable effect on the induction of interferon-stimulated genes or the activation of global RNA cleavages by RNase L. Moreover, we demonstrate that NoV infection of adult mice induces production of abundant vsiRNA active to guide RNA slicing by Argonaute-2. Notably, VSR-B2 suppresses the biogenesis of both vsiRNA and the slicing-competent vsiRNA-Argonaute-2 complex without detectable inhibition of Argonaute-2 slicing guided by endogenous microRNA, which dramatically enhances viral load and promotes lethal NoV infection in adult mice either intact or defective in the signaling by type I, II, and III interferons. Together, our findings suggest that the mouse RNAi response confers essential protective antiviral immunity in both the presence and absence of the interferon response.

Indexed as

RNA InterferenceVirus ReplicationAnimalsArgonaute ProteinsCell LineCells, CulturedDEAD-box RNA HelicasesFemaleFibroblastsMaleMiceMice, Inbred C57BLNodaviridaeRibonuclease IIIRNA, Double-StrandedRNA, Small InterferingAgo2 protein, mouseArgonaute ProteinsDEAD-box RNA HelicasesDicer1 protein, mouseRibonuclease IIIRNA, Double-StrandedRNA, Small Interferingantiviral RNAiinterferonsplus-strand RNA virusRNA interferenceviral suppressor of RNAi

Identifiers

PMID32753500
PMCPMC7407090
OpenAlexW3047244317

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.