Evidence map›Paper›PMID 38139259›Full record

ArticleInternational journal of molecular sciences2023

RSV Induces Activation of Intracellular EGFR on the Mitochondrial Membrane for Virus Propagation.

Se Sil Noh, Hye Jin Shin

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 38% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

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    Article
  2. Review
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

2 authors at 1 institution in 1 country.

Se Sil NohDepartment of Microbiology, School of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Hye Jin ShinDepartment of Microbiology, School of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Chungnam National University · KR

Funding

BK 21 FOUR Program Chungnam National University Research Grant, 2023National Research Foundation of Korea (NRF) grant Korean Government (MIST) (No. RS-2023-00248135)
6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) infects people of all ages and is one of the most common causative agents of lower respiratory tract infections, such as pneumonia, especially in infants under one year of age. However, no direct treatment has been developed for RSV infections. Maintenance of mitochondrial homeostasis and epidermal growth factor receptor (EGFR) activity is important for human cell growth. This study reported that RSV infection maintained the total cellular ATP levels and promoted the intracellular activity of EGFR to replicate RSV. RSV activates the intracellular EGFR-mediated cell survival signaling cascade and maintains mitochondrial EGFR expression for viral production during early events after infection. The approved EGFR inhibitor, vandetanib, markedly reduces RSV propagation, suggesting that EGFR is an attractive host target for RSV therapeutics. Our results suggest that RSV infection maintains cellular ATP levels and promotes the activation of intracellular EGFR in the mitochondrial membrane, significantly contributing to robust RSV propagation.

Indexed as

Respiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsAdenosine TriphosphateErbB ReceptorsHumansInfantMitochondrial MembranesAdenosine TriphosphateEGFR protein, humanErbB Receptorsintracellular epidermal growth factor receptormitochondrial homeostasisrespiratory syncytial virusvandetanib

Identifiers

PMID38139259
PMCPMC10744162
OpenAlexW4389680407

What OpenQuestion holds

Textmetadata
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.