Vanin-1 deficiency enhances host tolerance to influenza infection by modulating cellular redox status

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ID: 318107
2026
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Abstract
Abstract Host survival during infection depends on the balance between pathogen resistance and tissue tolerance mechanisms. Although resistance pathways are well-characterized, the molecular determinants of host tolerance remain poorly understood. Here we demonstrate that vanin-1, an ectoenzyme known for its role in vitamin B5 metabolism, unexpectedly regulates host tolerance during influenza infection through modulation of cellular redox status. Mice lacking vanin-1 showed enhanced survival following lethal influenza infection without alterations in viral burden, immune responses, or tissue pathology. While vanin-1 deficiency impairs vitamin B5 metabolism, neither vitamin B5 supplementation nor deficiency affected survival during infection, indicating a vitamin B5- independent mechanism. RNA sequencing analysis revealed enhanced expression of antioxidant pathway genes in vanin-1-deficient mice, with Nrf2 serving as a key upstream regulator. Mechanistically, vanin-1-deficient mice maintained higher glutathione levels during infection and showed reduced lipid peroxidation, suggesting protection against oxidative stress-induced cell death. Importantly, pharmacological inhibition of glutathione synthesis abolished the survival advantage in vanin-1-deficient mice, while glutathione supplementation protected wild-type mice from lethal infection. Our findings reveal an unexpected role for vanin-1 in regulating host tolerance through antioxidant pathways and identify a potential therapeutic target for enhancing survival during severe viral infections.
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Authors Jin Soo Joo, Lesley Pasman, Shuang Yu, Robert Homer, Philippe Naquet, Ruslan Medzhitov, Jun Young Hong
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Journal PNAS nexus
Year 2026
DOI
10.1093/pnasnexus/pgag222
URL
https://doi.org/10.1093/pnasnexus/pgag222
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