Evidence map›Paper›PMID 42731638›Full record

ArticleVirus research2026

The murine correlate of the Epstein-Barr and Kaposi's sarcoma-associated γ-herpesviruses, MHV-68, represents a valuable model to assess antiviral drug sensitivity and combinatorial drug synergies.

Christina Wangen, Debora Obergfäll, Katarína Briestenská, Jela Mistríková, William D Rawlinson, Manfred Marschall

Abstract read
In one paragraph

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

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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Christina WangenHarald zur Hausen Institute of Virology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Electronic address: christina.wangen@uk-erlangen.de.
Debora ObergfällHarald zur Hausen Institute of Virology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Electronic address: debora.obergfaell@fau.de.
Katarína BriestenskáDepartment of Microbiology and Virology, Faculty of Natural Sciences, Comenius University in Bratislava, Ilkovičova 6, Bratislava, 842 15, Slovakia; Institute of Virology, Biomedical Research Center, Slovak Academy of Sciences, Dúbravská cesta 9, Bratislava, 845 05, Slovakia. Electronic address: katarina.briestenska@savba.sk.
Jela MistríkováDepartment of Microbiology and Virology, Faculty of Natural Sciences, Comenius University in Bratislava, Ilkovičova 6, Bratislava, 842 15, Slovakia; Institute of Virology, Biomedical Research Center, Slovak Academy of Sciences, Dúbravská cesta 9, Bratislava, 845 05, Slovakia. Electronic address: jela.mistrikova@savba.sk.
William D RawlinsonSerology and Virology Division, NSW Health Pathology Microbiology, Prince of Wales Hospital, and Schools of Women's and Children's Health, Medicine and Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, Australia. Electronic address: w.rawlinson@unsw.edu.au.
Manfred MarschallHarald zur Hausen Institute of Virology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany. Electronic address: manfred.marschall@fau.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human herpesviruses represent major human pathogens. Members of the γ-Herpesvirinae subfamily are of particular interest because they cause chronic diseases, such as cancers, by altering cellular processes and driving resting cells into a continuously proliferating phase. Also, autoimmune diseases such as multiple sclerosis have continuously been in the focus of interest. The prototypic human γ-herpesvirus, Epstein-Barr virus (EBV), has proven difficult to analyze for the development of antiviral therapies due to challenges associated with propagating the virus in vitro, phenotyping it, and assessment of antiviral phenotypic efficacy. Similarly, developing experimental systems to study the second human pathogenic virus in this subfamily, Kaposi sarcoma-associated herpesvirus (KSHV), has been challenging. The murine γ-herpesvirus 68 (MHV-68) is a well-characterized homolog of EBV and KSHV and represents a model virus for cell culture-based and animal-specific analyses. Here, we used MHV-68 to determine virus sensitivity to antivirals, and combinatorial drug synergies. Much of the recent information about novel antiherpesviral drugs has come from studies of human cytomegalovirus (HCMV). Therefore, a comparative analysis was also conducted between HCMV, MHV-68, and EBV. The study demonstrated: (i) successful establishment of a new MHV-68 replication model in murine and non-murine cell types; (ii) optimization of an MHV-68-specific quantitative readout based on the luciferase reporter system; (iii) assessment of mechanistically novel antiherpesviral compounds; (iv) comparative antiviral effects spanning the three respective herpesviruses; (v) analysis of antiviral drug combination treatments able to identify statistically significant drug synergies. Overall, the study provides new insights into molecular aspects of γ-herpesvirus replication, as well as antiviral drug development and targeting strategies.

Indexed as

Assessment of antiviral drug sensitivityCombinatorial drug synergiesLuciferase reporter expressionModel of Epstein-Barr virus infectionMurine γ-herpesvirus 68 (MHV-68)Novel options of broad antiherpesviral targetingReplication in host cell types

Identifiers

PMID42731638
PMCPMC13602032

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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.