Evidence map›Paper›PMID 42662995›Full record

ReviewVirus evolution2026

Antagonistic co-evolution throughout the herpesvirus life cycle.

Thomas Höfler, Dina Aly Abdulrahman, Jana Reich, Lisa Kossak, Jenny Ospina-Garcia, Dilan Gün Serdar, Mariana Mara Nascimento, Yingnan Cheng, Benedikt Bertold Kaufer, Jakob Trimpert

Abstract readReview
In one paragraph

Review in Virus evolution, 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

10 authors.

Thomas HöflerDepartment of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University, 1800 Denison Avenue, Mosier Hall, 66506, Manhattan, KS, United States.ORCID https://orcid.org/0000-0001-7486-5582
Dina Aly AbdulrahmanInstitut für Virologie, Fachbereich Veterinärmedizin, Freie Universität Berlin, Robert-von-Ostertag Straße 7-13, Ge-bäude 35, 14163, Berlin, Germany.
Jana ReichInstitut für Virologie, Fachbereich Veterinärmedizin, Freie Universität Berlin, Robert-von-Ostertag Straße 7-13, Ge-bäude 35, 14163, Berlin, Germany.
Lisa KossakInstitut für Virologie, Fachbereich Veterinärmedizin, Freie Universität Berlin, Robert-von-Ostertag Straße 7-13, Ge-bäude 35, 14163, Berlin, Germany.
Jenny Ospina-GarciaInstitut für Virologie, Fachbereich Veterinärmedizin, Freie Universität Berlin, Robert-von-Ostertag Straße 7-13, Ge-bäude 35, 14163, Berlin, Germany.
Dilan Gün SerdarInstitut für Virologie, Fachbereich Veterinärmedizin, Freie Universität Berlin, Robert-von-Ostertag Straße 7-13, Ge-bäude 35, 14163, Berlin, Germany.
Mariana Mara NascimentoInstitut für Virologie, Fachbereich Veterinärmedizin, Freie Universität Berlin, Robert-von-Ostertag Straße 7-13, Ge-bäude 35, 14163, Berlin, Germany.
Yingnan ChengInstitut für Virologie, Fachbereich Veterinärmedizin, Freie Universität Berlin, Robert-von-Ostertag Straße 7-13, Ge-bäude 35, 14163, Berlin, Germany.
Benedikt Bertold KauferInstitut für Virologie, Fachbereich Veterinärmedizin, Freie Universität Berlin, Robert-von-Ostertag Straße 7-13, Ge-bäude 35, 14163, Berlin, Germany.
Jakob TrimpertDepartment of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University, 1800 Denison Avenue, Mosier Hall, 66506, Manhattan, KS, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Herpesviruses are a widespread and diverse family of large double-stranded DNA viruses. Narrow host ranges maintained over long evolutionary times have fostered intimate host adaptations. However, such close virus-host associations inevitably invite conflict. Genetic conflict describes antagonistic interactions between two individuals that drive genetic changes to overcome said conflict. During the herpesvirus infectious cycle, genetic conflict-and specifically antagonistic co-evolution-can occur on multiple levels: between host and virus, between co-infecting viruses, or between genes within the same genome. This review highlights the many ways such conflict occurs and how it shapes herpesvirus evolution. Starting with attachment and entry, and continuing through gene expression, DNA metabolism, packaging, and egress, we examine how antagonistic interactions manifest at each stage of the viral life cycle. Latency and immunity receive special consideration as their inherent biology makes them focal points of sustained antagonism. Since genetic conflict is a major force in evolutionary ecology, we aim to emphasize its central role in herpesvirus biology and encourage future studies to explicitly consider the antagonistic forces shaping their evolution.

Indexed as

antiviral immunityevolutiongenetic conflictherpesviruseslatencyvirus-virus interaction

Identifiers

PMID42662995
PMCPMC13521526

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.