Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The c-Rel transcription factor limits early interferon and neuroinflammatory responses to prevent herpes simplex encephalitis onset in mice.

Scientific reports - 27 Oct 2021

Mancini Mathieu, Charbonneau Benoît, Langlais David, Vidal Silvia M

Abstract excerpt

Herpes simplex virus type 1 (HSV-1) is the predominant cause of herpes simplex encephalitis (HSE), a condition characterized by acute inflammation and viral replication in the brain. Host genetics contribute to HSE onset, including monogenic defects in type I interferon signaling in cases of childhood HSE. Mouse models suggest a further contribution of immune cell-mediated inflammation to HSE pathogenesis. We...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Interferon Type I
Share to Mice
Share to Mice, Inbred C57BL

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mutation

Share to Proto-Oncogene Proteins c-rel

Share to Signal Transduction

Share to Simplexvirus

Share to T-Lymphocytes

Source

Open in PubMed Open full text

Identifiers

PMID: 34707143
DOI: 10.1038/s41598-021-00391-7
PMCID: PMC8551191

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The c-Rel transcription factor limits early interferon and neuroinflammatory responses to prevent herpes simplex encephalitis onset in mice.PMID 34707143Read ↗

Insights into the pathogenesis of herpes simplex encephalitis from mouse models.Semantic proximity Read ↗

Genetic susceptibility to herpes simplex virus 1 encephalitis in mice and humans.Semantic proximity Read ↗

Temporally resolved single-cell RNA sequencing reveals protective and pathological responses during herpes simplex virus 1 CNS infectionSemantic proximity Read ↗

Functional Genomics Reveals an Essential and Specific Role for Stat1 in Protection of the Central Nervous System following Herpes Simplex Virus Corneal InfectionSemantic proximity Read ↗

Herpes simplex encephalitis in a patient with a distinctive form of inherited IFNAR1 deficiencySemantic proximity Read ↗

Cutting edge: a NK complex-linked locus governs acute versus latent herpes simplex virus infection of neurons.Semantic proximity Read ↗

Intranasal HSV-1 Infection Drives Region-Specific Interferon-Dominant Microglial RemodelingSemantic proximity Read ↗

High-resolution spatial transcriptomics maps viral tropism and reveals spatially organized immune modules in viral encephalitisSemantic proximity Read ↗

The histone chaperone HIRA promotes the induction of host innate immune defences in response to HSV-1 infectionSemantic proximity Read ↗

Herpes simplex virus encephalitis of childhood: inborn errors of central nervous system cell-intrinsic immunity.Semantic proximity Read ↗

Interferon-α and -β subtypes have temporally distinct roles in containing viral spread and protecting vital organsSemantic proximity Read ↗

Mendelian predisposition to herpes simplex encephalitis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.