ReviewNature2024
Genetic defects of brain immunity in childhood herpes simplex encephalitis.
Review in Nature, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Clinical phenotype and outcomes in autoimmune encephalitis after herpes simplex virus encephalitis: A systematic review and meta-analysis.The Journal of infection · 2025Pooled it
- The cell-type-specific roles of Toll-like receptors in herpes simplex virus infection and pathogenesis.Virulence · 2026Review
- Herpes simplex virus pUL56 abolishes neuronal activity by removing voltage-gated ion channels from the plasma membrane.Science advances · 2026Article
- Host Genetic Susceptibility and Antiviral Immunity Shape the Pathogenesis and Outcomes of Herpes Simplex Encephalitis.Biology · 2026Review
- Inherited human TFIIIA deficiency disrupts T cell development.medRxiv : the preprint server for health sciences · 2026Article
- Toward a monogenic architecture of human infections: From 1996 to 2026.Journal of human immunity · 2026Review
- Clinical and laboratory profiles of acute central nervous system infections in a Chinese pediatric cohort: a five-year retrospective analysis.BMC pediatrics · 2026Article
- Cepharanthine hydrochloride alleviates herpesvirus encephalitis by inhibiting Nrf2 degradation.Virologica Sinica · 2026Article
- Recurrent severe viral infection in a child with inherited complete TBK1 deficiency.Journal of human immunity · 2026Article
- Human inborn errors of the alternative NF-κB pathway.Journal of human immunity · 2026Review
- Role for NF-κB in herpes encephalitis pathology in mice genocopying an inborn error of IRF3-IFN immunity.The Journal of experimental medicine · 2026Article
- The cell-mediated adaptive immune response to herpes simplex virus type 1 encephalitis: mechanisms and clinical implications.Frontiers in immunology · 2026Review
- Innate immune signalling, neuroinflammation and network plasticity in temporal lobe epilepsy.Frontiers in pharmacology · 2026Review
- Zyxin restricts viral fusion and entry across multiple virus families.Journal of virology · 2025Article
- Review
- Fatal hemorrhagic leukoencephalitis following VZV reactivation in an immunocompetent host: a case report.Journal of neurology · 2025Article
- Human inborn errors of type I interferon-independent intrinsic immunity in nonleukocytic cells.Current opinion in immunology · 2025Review
- Research trends on herpes simplex encephalitis in children: a bibliometric analysis from 1975 to 2024.Translational pediatrics · 2025Article
- Interferons in health and disease.Cell · 2025Review
- IRF1 amplifies HSV-1-triggered antiviral innate immunity in a feed-forward manner.Cell insight · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Herpes simplex virus 1 (HSV-1) encephalitis (HSE) is the most common sporadic viral encephalitis in humans. It is life-threatening and has a first peak of incidence in childhood, during primary infection. Children with HSE are not particularly prone to other infections, including HSV-1 infections of tissues other than the brain. About 8-10% of childhood cases are due to monogenic inborn errors of 19 genes, two-thirds of which are recessive, and most of which display incomplete clinical penetrance. Childhood HSE can therefore be sporadic but genetic, enabling new diagnostic and therapeutic approaches. In this Review, we examine essential cellular and molecular mechanisms of cell-intrinsic antiviral immunity in the brain that are disrupted in individuals with HSE. These mechanisms include both known (such as mutations in the TLR3 pathway) and previously unknown (such as the TMEFF1 restriction factor) antiviral pathways, which may be dependent (for example, IFNAR1) or independent (for example, through RIPK3) of type I interferons. They operate in cortical or brainstem neurons, and underlie forebrain and brainstem infections, respectively. Conversely, the most severe inborn errors of leukocytes, including a complete lack of myeloid and/or lymphoid blood cells, do not underlie HSE. Thus congenital defects in intrinsic immunity in brain-resident neurons that underlie HSE broaden natural host defences against HSV-1 from the leukocytes of the immune system to other cells in the organism.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.