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July 31, 2014PLoS ONEOpen Access

mRNA Decay Factor AUF1 Binds the Internal Ribosomal Entry Site of Enterovirus 71 and Inhibits Virus Replication

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Population

Cells infected with enterovirus 71 (EV71)

Comparison

AUF1 knockdown vs Mock-infected cells or cells without AUF1…

Design

Preclinical

Authors

JLJing‐Yi LinMLMei-Ling LiGBGary Brewer

Discussion

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Overview

AUF1 may restrict EV71 in cell models; hypothesis-generating for host-targeted antivirals, with no immediate clinical implications.

Structured PICO

P
Population
Cells infected with enterovirus 71 (EV71)
I
Intervention
AUF1 knockdown
C
Comparator
Mock-infected cells or cells without AUF1 knockdown
O
Outcome
IRES-dependent translation and viral replication

AUF1 binds the EV71 IRES and negatively regulates viral translation and replication, identifying a potential host restriction factor for EV71.

Cite This Study

Lin et al. (2014) studied this question.

synapsesocial.com/papers/6a718881f44fa9f079df504chttps://doi.org/10.1371/journal.pone.0103827
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Cellular mRNA Decay Protein AUF1 Negatively Regulates Enterovirus and Human Rhinovirus Infections2013 · 67 citations
  2. 2Far upstream element binding protein 2 interacts with enterovirus 71 internal ribosomal entry site and negatively regulates viral translation2008 · 148 citations
  3. 3Picornavirus Modification of a Host mRNA Decay Protein2012 · 61 citations
  4. 4An Epidemic of Enterovirus 71 Infection in Taiwan1999 · 1,174 citations
  5. 5Far upstream element binding protein 1 binds the internal ribosomal entry site of enterovirus 71 and enhances viral translation and viral growth2011 · 79 citations