ArticleJournal of immunology (Baltimore, Md. : 1950)2024
High-Affinity-Mediated Viral Entry Triggers Innate Affinity Escape Resulting in Type I IFN Resistance and Impaired T Cell Immunity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Lymphocytic Choriomeningitis Virus Bearing GPC Mutations for Enhanced Tumor Tropism and Strong Anti-Tumor Activity.Viruses · 2026Article
- Article
- Sulfated glycosaminoglycans inhibit LCMV entry and modulate antiviral immunity and pathology.EMBO molecular medicine · 2026Article
- Identification and genomic characterization of BA.3.2: a highly divergent BA.3-related SARS-CoV-2 lineage from southern Africa.Virus evolution · 2026Article
- Optimized arenaviruses with tumor-tropic mutations promote safe anti-tumor efficacy via sustainable immune modulatory properties.Cell reports. Medicine · 2025Article
- Myoglobin expression improves T-cell metabolism and antitumor effector function.Journal for immunotherapy of cancer · 2025Article
- Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Increased receptor binding affinity may allow viruses to escape from Ab-mediated inhibition. However, how high-affinity receptor binding affects innate immune escape and T cell function is poorly understood. In this study, we used the lymphocytic choriomeningitis virus (LCMV) murine infection model system to create a mutated LCMV exhibiting higher affinity for the entry receptor α-dystroglycan (LCMV-GPH155Y). We show that high-affinity receptor binding results in increased viral entry, which is associated with type I IFN (IFN-I) resistance, whereas initial innate immune activation was not impaired during high-affinity virus infection in mice. Consequently, IFN-I resistance led to defective antiviral T cell immunity, reduced type II IFN, and prolonged viral replication in this murine model system. Taken together, we show that high-affinity receptor binding of viruses can trigger innate affinity escape including resistance to IFN-I resulting in prolonged viral replication.
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Registered trials
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