ArticleFrontiers in immunology2026
Roles of sex and SP-A genetic variants in modulating multiorgan injuries post viral infection.
Article in Frontiers in immunology, 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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Abstract
Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), and multi-organ dysfunction (MOD). Human surfactant protein A (SP-A), a key component of innate immunity, exhibits genetic polymorphisms that may influence host responses to viral infection. Human patient studies have shown that biological sex has been associated with differences in COVID-19 severity. However, the combined effects of SP-A variants and sex on SARS-CoV-2-induced organ injury remain poorly understood. Methods: We utilized double-humanized transgenic mice expressing human ACE2 and individual human SP-A variants (6A Results: SP-A variants significantly attenuated SARS-CoV-2-induced organ injury compared to KO mice, with SP-A variant and organ-specific effects. In the lung, injury severity followed the order 6A Conclusions: Human SP-A genetic variants and biological sex interact to modulate SARS-CoV-2-induced multi-organ injury in a tissue-specific manner. These findings highlight the importance of host genetic variation in innate immunity and suggest that SP-A variants, together with sex-specific considerations, may inform risk stratification and therapeutic strategies for COVID-19 and related viral diseases.
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