Evidence map›Paper›PMID 27528682›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Cell autonomous regulation of herpes and influenza virus infection by the circadian clock.

Rachel S Edgar, Alessandra Stangherlin, Andras D Nagy, Michael P Nicoll, Stacey Efstathiou, John S O'Neill, Akhilesh B Reddy

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 1% 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

149 citing papers in PubMed, 1 synthesis or guideline pooled it, 234 citations in OpenAlex.

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  10. A circadian checkpoint relocates neutrophils to minimize injury.The Journal of experimental medicine · 2026
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  16. The βScience advances · 2025
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89 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

Rachel S EdgarUniversity of Cambridge Metabolic Research Laboratories, Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, United Kingdom;
Alessandra StangherlinUniversity of Cambridge Metabolic Research Laboratories, Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, United Kingdom;
Andras D NagyUniversity of Cambridge Metabolic Research Laboratories, Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, United Kingdom; Department of Anatomy, University of Pecs Medical School, H-7624 Pecs, Hungary;
Michael P NicollDivision of Virology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom.
Stacey EfstathiouDivision of Virology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom.
John S O'NeillUniversity of Cambridge Metabolic Research Laboratories, Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, United Kingdom;
Akhilesh B ReddyUniversity of Cambridge Metabolic Research Laboratories, Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, United Kingdom; areddy@cantab.net.
University of Cambridge · GBWellcome/MRC Institute of Metabolic Science · GBMedical Research Council · GBWellcome Trust · GB

Funding

Medical Research Council MC_UP_1201/4Wellcome Trust
6 · The paper itself

Abstract

Viruses are intracellular pathogens that hijack host cell machinery and resources to replicate. Rather than being constant, host physiology is rhythmic, undergoing circadian (∼24 h) oscillations in many virus-relevant pathways, but whether daily rhythms impact on viral replication is unknown. We find that the time of day of host infection regulates virus progression in live mice and individual cells. Furthermore, we demonstrate that herpes and influenza A virus infections are enhanced when host circadian rhythms are abolished by disrupting the key clock gene transcription factor Bmal1. Intracellular trafficking, biosynthetic processes, protein synthesis, and chromatin assembly all contribute to circadian regulation of virus infection. Moreover, herpesviruses differentially target components of the molecular circadian clockwork. Our work demonstrates that viruses exploit the clockwork for their own gain and that the clock represents a novel target for modulating viral replication that extends beyond any single family of these ubiquitous pathogens.

Indexed as

Host-Pathogen InteractionsAnimalsARNTL Transcription FactorsBiological TransportCell LineChromatin Assembly and DisassemblyCircadian ClocksCircadian RhythmCLOCK ProteinsCricetinaeEpithelial CellsFemaleGene Expression RegulationGenes, ReporterHerpes SimplexHerpesviridae InfectionsARNTL Transcription FactorsBmal1 protein, mouseClock protein, mouseCLOCK ProteinsLuciferasescircadianclockherpesinfluenzavirus

Identifiers

PMID27528682
PMCPMC5018795
OpenAlexW2512516821

What OpenQuestion holds

Textmetadata
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.