ArticleiScience2026
Extensive evolution and T cell escape by SARS-CoV-2 in a 2.5-year persistent infection of an immunocompromised host.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
11 authors.
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Abstract
Prolonged virus-host interaction and suboptimal immunity during persistent SARS-CoV-2 infection of immunocompromised patients enables viral adaptation. We investigated viral evolution and immune escape during a 2.5-year persistent infection in a patient with multiple myeloma and rheumatoid arthritis receiving anti-CD20 therapy. Virus isolated 899-days post-infection revealed an ancestral B.31 lineage with extensive evolution (56 non-synonymous mutations across 20 viral proteins). Many mutations were private or convergent with those seen in other persistent infections and later variants. SARS-CoV-2-specific antibodies were undetectable. Despite prolonged antigen exposure, T cell memory was functional high-in-magnitude and breadth, but with inhibitory receptor expression and dominant spike-specific CD8 response. 38/56 mutations occurred in T cell epitopes, reducing MHC binding or immunogenicity for 69% of CD8 epitopes affected. Importantly, functional assays confirmed T cell escape at 50% (1/2) and 86% (6/7) of CD8 and CD4 epitopes tested
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