Authors
Julie A Jensen, Morten Kelder Skouboe, Adrian Gervais, Sofie Eg Jørgensen, Nanna Mørk, Marvin Werner, Renée M van der Sluis, Bettina Bundgaard, Jacob Bodilsen, Paul Bastard, Muyesier Maimaitili, Stefanie Fruhwürth, Marie Helleberg, Merete Storgaard, Henrik Nielsen, Anne Puel, Shen-Ying Zhang, Søren R Paludan, Aurelie Cobat, Jean-Laurent Casanova, Trine H Mogensen
Published in
The Journal of experimental medicine. Volume 223. Issue 10. Oct 05, 2026. Epub Sep 28, 2026.
Abstract
Inborn errors of type I interferon (IFN-I) immunity account for ∼7-8% of herpes simplex encephalitis (HSE) cases in young children, but the pathogenesis of HSE in adults is largely unknown. We report that IFN-I autoantibodies (auto-Abs) in serum/plasma samples drawn before, during, or after HSE in 16/339 Danish adults neutralized 0.1-10 ng/ml of IFN-I. Neutralization was IgG-mediated and was also detected in cerebrospinal fluid in several patients. Patients' serum impaired the ability of exogenous IFN-I to protect fibroblasts against herpes simplex virus (HSV)-1 infection in vitro. Among patients with neutralizing IFN-I auto-Abs, a larger fraction were HSV-1 IgG seronegative, suggesting that these auto-Abs confer a greater risk of HSE during primary HSV-1 infection. Neutralization was mainly driven by auto-Abs to IFN-ω, and the risk of HSE in adults with auto-Abs was significantly elevated (odds ratio [OR] = 3.1 for IFN-ω and OR = 2.0 for any IFN-I) compared with the general population. Overall, auto-Abs neutralizing IFN-I accounted for ∼5% of adult HSE cases.
PMID:
42803734
Bibliographic data and abstract were imported from PubMed on 28 Sep 2026.
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