Evidence map›Paper›PMID 41965674›Full record

ArticleVirology journal2026

Poxvirus infection triggers remodeling of host m⁶A epitranscriptome and benefits from the m⁶A regulatory responses.

Taehyung Kwon, Demosthenes P Morales, Abigale S Mikolitis, Phillip M Mach, Cheryl D Gleasner, Sofiya N Micheva-Viteva

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virology journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Taehyung KwonBiochemistry and Biotechnology Group (B-TEK), Bioscience Division, Los Alamos National Laboratory, Los Alamos, NM, USA.
Demosthenes P MoralesCenter for Integrated Nanotechnologies (MPA-CINT), Los Alamos National Laboratory, Los Alamos, NM, USA.
Abigale S MikolitisBiochemistry and Biotechnology Group (B-TEK), Bioscience Division, Los Alamos National Laboratory, Los Alamos, NM, USA.
Phillip M MachBiochemistry and Biotechnology Group (B-TEK), Bioscience Division, Los Alamos National Laboratory, Los Alamos, NM, USA.
Cheryl D GleasnerGenomics and Bioanalytics Group (B-GEN), Bioscience Division, Los Alamos National Laboratory, Los Alamos, NM, USA.
Sofiya N Micheva-VitevaBiochemistry and Biotechnology Group (B-TEK), Bioscience Division, Los Alamos National Laboratory, Los Alamos, NM, USA. sviteva@lanl.gov.

Funding

Laboratory Directed Research and Development program of Los Alamos National Laboratory 20230167ERU.S. Defense Threat Reduction Agency HDTRA1447547
6 · The paper itself

Abstract

backgroundUnderstanding how host gene regulation responds to viral infection is essential for developing effective antiviral strategies. Emerging evidence suggests that host transcripts undergo dynamic chemical modifications to counteract viral invasion. Conversely, viruses that rely on nuclear transcription exploit host RNA methyltransferases to enhance mRNA export and translation. Orthopoxviruses, however, complete their entire replication cycle within compartmentalized cytoplasmic "factories" utilizing enzymes encoded by their large double-stranded viral DNA genomes. The dynamic interplay between host and poxviral epitranscriptome remains poorly characterized.

resultsUsing a temporally resolved model of Vaccinia virus (VV) infection, we investigated host-virus interactions through transcriptome and N6-methyladenosine (m⁶A) epitranscriptome whole genome sequencing. We found that host m⁶A modifications respond rapidly to VV infection, preceding the delayed transcriptional changes that emerge at later stages. Early m⁶A signatures included key innate immunity factors as well as host genes involved in transcriptional regulation, post-transcriptional modification, and protein ubiquitination. Functional assays validated two host factors with early m⁶A modification changes that are essential for VV infection: a m⁶A reader, YTHDF1, and a component of the SCF E3 ubiquitin ligase complex, FBXO31. The m⁶A gain on YTHDF1 enhanced its protein expression and promoted efficient VV replication. In addition, we identified previously unrecognized roles of FBXO31 and the SCF E3 ligase complex in supporting VV infection.

conclusionTemporal profiling of the m⁶A epitranscriptome reveals how VV exploits host post-transcriptional regulatory pathways, specifically m⁶A RNA modification and protein ubiquitination. These findings highlight critical host factors co-opted during poxvirus infection and identify potential targets for therapeutic intervention.

Indexed as

AdenosineHost-Pathogen InteractionsVacciniaVaccinia virusCell LineEpitranscriptomeEpitranscriptomicsGene Expression RegulationHumansRNA-Binding ProteinsRNA MethylationTranscriptomeVirus ReplicationAdenosineN-methyladenosineRNA-Binding ProteinsHost-virus interactionm⁶A epitranscriptomePost-transcriptional regulationTemporal transcriptomicsVaccinia virusYTHDF1

Identifiers

PMID41965674
PMCPMC13202759

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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.