Authors
Maki Taniguchi, Chiaki Tao, Takaki Asano, Miyuki Tsumura, Ko Ko, Hiroko Kumada, Takanori Utsumi, Kosuke Noma, Fumiaki Sakura, Kosuke Ashihara, Moe Tamaura, Yoko Mizoguchi, Osamu Ohara, Dusan Bogunovic, Paul Bastard, Jean-Laurent Casanova, Junko Tanaka, Masataka Tsuge, Kazuaki Chayama, Shiro Oka, Satoshi Okada
Published in
Journal of human immunity. Volume 2. Issue 6. Nov 02, 2026. Epub Sep 16, 2026.
Abstract
Autoantibodies neutralizing type I IFNs (AAN-I-IFNs) are being identified as major, common, and global determinants of a growing range of severe viral diseases. We examined whether persistent hepatitis C virus (HCV) infection, with or without IFN-α therapy, could induce AAN-I-IFNs. We tested 2,573 HCV patients aged 1-95 years (1,115 treated with IFN-α, 1,458 untreated) and 1,000 healthy controls. AAN-INF-α2 prevalence was significantly higher in hepatitis C patients (2.7%) than in healthy controls (0.7%) and was higher still in those treated with IFN-α (3.9%) than in untreated patients (1.9%) (P = 0.0053). A longitudinal study of 15 IFN-α-treated patients with AAN-IFN-α2 revealed that only one had AAN-IFN-α2 before IFN-α therapy and that 12 patients developed AAN-IFN-α2 in the year following treatment. However, 80% eventually became AAN-IFN-α2 negative. These findings suggest that chronic HCV infection, perhaps due to the chronic production of endogenous IFN-α, and exogenous IFN-α treatment promote the development of AAN-IFN-α2.
PMID:
42747404
Bibliographic data and abstract were imported from PubMed on 16 Sep 2026.
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