ArticleAllergy2021
Whole genome sequencing identifies novel genetic mutations in patients with eczema herpeticum.
Article in Allergy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Disease-linked regulatory DNA variants and homeostatic transcription factors in epidermis.Nature communications · 2025Article
- The mRNA and microRNA Landscape of the Blastema Niche in Regenerating Newt Limbs.International journal of molecular sciences · 2024Article
- Development of a Risk Prediction Model for Adverse Skin Events Associated with TNF-α Inhibitors in Rheumatoid Arthritis Patients.Journal of clinical medicine · 2024Article
- Atopic Dermatitis Complicated by Recurrent Eczema Herpeticum Is Characterized by Multiple, Concurrent Epidermal Inflammatory Endotypes.JID innovations : skin science from molecules to population health · 2024Article
- Genetic and Immunological Pathogenesis of Atopic Dermatitis.The Journal of investigative dermatology · 2024Review
- Novel insights into atopic dermatitis.The Journal of allergy and clinical immunology · 2023Review
- Incorporating genetics in identifying peanut allergy risk and tailoring allergen immunotherapy: A perspective on the genetic findings from the LEAP trial.The Journal of allergy and clinical immunology · 2023Review
- Epidermal differentiation complex genetic variation in atopic dermatitis and peanut allergy.The Journal of allergy and clinical immunology · 2023Article
- Inborn Errors of Immunity Predisposing to Herpes Simplex Virus Infections of the Central Nervous System.Pathogens (Basel, Switzerland) · 2023Review
- The Genetics of Eczema Herpeticum.Clinical reviews in allergy & immunology · 2022Review
- Resolution of Eczema with Multivalent Peptides.JID innovations : skin science from molecules to population health · 2022Article
- The Discovery and Function of Filaggrin.International journal of molecular sciences · 2022Review
- Genetic/Environmental Contributions and Immune Dysregulation in Children with Atopic Dermatitis.Journal of asthma and allergy · 2022Review
- Whole-genome sequencing in diverse subjects identifies genetic correlates of leukocyte traits: The NHLBI TOPMed program.American journal of human genetics · 2021Article
- Update on the pathogenesis of atopic dermatitis.Anais brasileiros de dermatologiaReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
28 authors at 11 institutions in 1 country.
Funding
Abstract
backgroundEczema herpeticum (EH) is a rare complication of atopic dermatitis (AD) caused by disseminated herpes simplex virus (HSV) infection. The role of rare and/or deleterious genetic variants in disease etiology is largely unknown. This study aimed to identify genes that harbor damaging genetic variants associated with HSV infection in AD with a history of recurrent eczema herpeticum (ADEH+).
methodsWhole genome sequencing (WGS) was performed on 49 recurrent ADEH+ (≥3 EH episodes), 491 AD without a history of eczema herpeticum (ADEH-) and 237 non-atopic control (NA) subjects. Variants were annotated, and a gene-based approach (SKAT-O) was used to identify genes harboring damaging genetic variants associated with ADEH+. Genes identified through WGS were studied for effects on HSV responses and keratinocyte differentiation.
resultsEight genes were identified in the comparison of recurrent ADEH+to ADEH-and NA subjects: SIDT2, CLEC7A, GSTZ1, TPSG1, SP110, RBBP8NL, TRIM15, and FRMD3. Silencing SIDT2 and RBBP8NL in normal human primary keratinocytes (NHPKs) led to significantly increased HSV-1 replication. SIDT2-silenced NHPKs had decreased gene expression of IFNk and IL1b in response to HSV-1 infection. RBBP8NL-silenced NHPKs had decreased gene expression of IFNk, but increased IL1b. Additionally, silencing SIDT2 and RBBP8NL also inhibited gene expression of keratinocyte differentiation markers keratin 10 (KRT10) and loricrin (LOR).
conclusionSIDT2 and RBBP8NL participate in keratinocyte's response to HSV-1 infection. SIDT2 and RBBP8NL also regulate expression of keratinocyte differentiation genes of KRT10 and LOR.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.