Comprehensive Mutagenesis of Herpes Simplex Virus 1 Genome Identifies UL42 as an Inhibitor of Type I Interferon Induction.

Maxime Chapon, Kislay Parvatiyar, Saba Roghiyh Aliyari, Jeffrey S Zhao, Genhong Cheng

Open access · bronzeAbstract read

In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it

0cells of the map it votes in

8citing papers in PubMed

1.1field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

Associations of viral infections and antiviral vaccinations with anti-NMDAR and other forms of autoimmune encephalitis.Brain, behavior, & immunity - health · 2026
Review
Alpha-herpesvirus US1 interacts with cGAS to suppress type I IFN responses and antiviral defense.PLoS pathogens · 2025
Article
Pseudorabies virus DNA polymerase processivity factor pUL42 inhibits type I IFN production by negatively regulating cGAS-STING signaling pathway.Journal of virology · 2025
Article
The producer cell type of HSV-1 alters the proteomic contents and infectious capacity of virions.Journal of virology · 2025
Article
Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis.Pathogens (Basel, Switzerland) · 2023
Review
The gamble between oncolytic virus therapy and IFN.Frontiers in immunology · 2022
Review
Evasion of I Interferon-Mediated Innate Immunity by Pseudorabies Virus.Frontiers in microbiology · 2021
Review
Herpes Simplex Virus Type 1 Interactions with the Interferon System.International journal of molecular sciences · 2020
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

5 authors at 1 institution in 1 country.

Maxime ChaponDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, USA.

Kislay ParvatiyarDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, USA.

Saba Roghiyh AliyariDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, USA.

Jeffrey S ZhaoDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, USA.

Genhong ChengDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, USA gcheng@mednet.ucla.edu.

University of California, Los Angeles · US

Funding

Viral Mediated Type I Interferon InductionR01AI069120 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHENG, GENHONG · 2006 to 2021

$6.0M

NIAID NIH HHS R01 AI069120

6 · The paper itself

Abstract

In spite of several decades of research focused on understanding the biology of human herpes simplex virus 1 (HSV-1), no tool has been developed to study its genome in a high-throughput fashion. Here, we describe the creation of a transposon insertion mutant library of the HSV-1 genome. Using this tool, we aimed to identify novel viral regulators of type I interferon (IFN-I). HSV-1 evades the host immune system by encoding viral proteins that inhibit the type I interferon response. Applying differential selective pressure, we identified the three strongest viral IFN-I regulators in HSV-1. We report that the viral polymerase processivity factor UL42 interacts with the host transcription factor IFN regulatory factor 3 (IRF-3), inhibiting its phosphorylation and downstream beta interferon (IFN-β) gene transcription. This study represents a proof of concept for the use of high-throughput screening of the HSV-1 genome in investigating viral biology and offers new targets both for antiviral therapy and for oncolytic vector design.

Indexed as

MutagenesisA549 CellsAntiviral AgentsDNA-Directed DNA PolymeraseExodeoxyribonucleasesHEK293 CellsHerpesvirus 1, HumanHumansInterferon-betaInterferon Regulatory Factor-3Interferon Type IReceptor, Interferon alpha-betaViral ProteinsAntiviral AgentsDNA-Directed DNA PolymeraseDNA polymerase, SimplexvirusExodeoxyribonucleasesIFNAR1 protein, humanInterferon-betaInterferon Regulatory Factor-3Interferon Type IIRF3 protein, humanReceptor, Interferon alpha-betaViral ProteinsHSV-1interferonIRF-3UL42

Identifiers

PMID31511375

DOI10.1128/JVI.01446-19

PMCPMC6854482

OpenAlexW2972742120

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.