Evidence map›Paper›PMID 31424151›Full record

ArticleCellular microbiology2019

Biphasic regulation of RNA interference during rotavirus infection by modulation of Argonaute2.

Urbi Mukhopadhyay, Shampa Chanda, Upayan Patra, Anupam Mukherjee, Satoshi Komoto, Mamta Chawla-Sarkar

Open access · bronzeAbstract read
In one paragraph

Article in Cellular microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
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  4. Frontiers in cellular and infection microbiology · 2025
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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

6 authors at 3 institutions in 2 countries.

Urbi MukhopadhyayDivision of Virology, National Institute of Cholera and Enteric Diseases, Kolkata, India.
Shampa ChandaDepartment of Biotechnology, GITAM Institute of Science, Visakhapatnam, India.
Upayan PatraDivision of Virology, National Institute of Cholera and Enteric Diseases, Kolkata, India.
Anupam MukherjeeDivision of Virology, National Institute of Cholera and Enteric Diseases, Kolkata, India.
Satoshi KomotoDepartment of Virology and Parasitology, School of Medicine, Fujita Health University, Aichi, Japan.
Mamta Chawla-SarkarDivision of Virology, National Institute of Cholera and Enteric Diseases, Kolkata, India.ORCID 0000-0002-7141-1785
National Institute of Cholera and Enteric Diseases · INFujita Health University · JPIndian Institute of Management Visakhapatnam · IN

Funding

Okayama University Project through Japan Initiative for Global Research Network on Infectious Diseases (J-GRID) of the Agency for Medical Research and Development (AMED)Science and Engineering Research Board; Dept. of Science and Technology (DST-SERB) EMR/2016/001361
6 · The paper itself

Abstract

RNA interference (RNAi) is an evolutionary ancient innate immune response in plants, nematodes, and arthropods providing natural protection against viral infection. Viruses have also gained counter-defensive measures by producing virulence determinants called viral-suppressors-of-RNAi (VSRs). Interestingly, in spite of dominance of interferon-based immunity over RNAi in somatic cells of higher vertebrates, recent reports are accumulating in favour of retention of the antiviral nature of RNAi in mammalian cells. The present study focuses on the modulation of intracellular RNAi during infection with rotavirus (RV), an enteric virus with double-stranded RNA genome. Intriguingly, a time point-dependent bimodal regulation of RNAi was observed in RV-infected cells, where short interfering RNA (siRNA)-based RNAi was rendered non-functional during early hours of infection only to be reinstated fully beyond that early infection stage. Subsequent investigations revealed RV nonstructural protein 1 to serve as a putative VSR by associating with and triggering degradation of Argonaute2 (AGO2), the prime effector of siRNA-mediated RNAi, via ubiquitin-proteasome pathway. The proviral significance of AGO2 degradation was further confirmed when ectopic overexpression of AGO2 significantly reduced RV infection. Cumulatively, the current study presents a unique modulation of host RNAi during RV infection, highlighting the importance of antiviral RNAi in mammalian cells.

Indexed as

AnimalsArgonaute ProteinsCell LineCell Line, TumorHaplorhiniHEK293 CellsHost-Pathogen InteractionsHT29 CellsHumansRNA, Double-StrandedRNA InterferenceRNA, Small InterferingRNA, ViralRotavirus InfectionsAGO2 protein, humanArgonaute ProteinsRNA, Double-StrandedRNA, Small InterferingRNA, ViralArgonaute2nonstructural protein 1RNA interferencerotavirusviral-suppressors-of-RNAi

Identifiers

PMID31424151
PMCPMC7162324
OpenAlexW2969582027

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Registered trials

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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.