Evidence map›Paper›PMID 41963616›Full record

ArticleCommunications biology2026

Human telomerase reverse transcriptase supports respiratory syncytial virus replication.

HoangDinh Huynh, Chien-Ting Wu, Jeffrey S Kahn

Abstract read
In one paragraph

Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

HoangDinh HuynhDepartment of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Chien-Ting WuDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Jeffrey S KahnDepartment of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA. Jeffrey.Kahn@UTSouthwestern.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Respiratory syncytial virus (RSV), discovered in 1956 and identified in children in 1957, is the major respiratory pathogen of infants and children under the age of 5 worldwide. RSV remains a significant challenge, despite recent advancements of vaccine development and monoclonal antibody prophylaxis. While specific antiviral agents have shown success as therapeutics for many other viruses, viral mutations inevitably develop, making these therapeutic interventions ineffective due to viral resistance. This unavoidable obstacle warrants alternative approaches to targeting host cellular factors that are essential for viral replication regardless of viral mutations. Our goal was to assess the feasibility of this approach. In doing so, we sought to determine the cellular enzymes and functions that are required for RSV replication. Here, we demonstrate that inhibiting human telomerase reduced or abolished viral protein production. Further, we showed that RNA helicase eIF4A is essential for RSV protein and progeny production. Lastly, targeting nuclear transport receptor reduces RSV RNAs and proteins synthesis, suggesting a role of host nucleus for viral replication. Overall, the inhibition of virus replication-dependent host functions may be an effective means to combat viral infections and would sidestep the inevitable resistance that emerges with virus-specific strategies.

Indexed as

Respiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsTelomeraseVirus ReplicationHost-Pathogen InteractionsHumansViral ProteinsTelomeraseTERT protein, humanViral Proteins

Identifiers

PMID41963616
PMCPMC13265742

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.