一种源自肠道的链球菌（Streptococcus dysgalactiae）通过细胞壁介导的病毒粒子物理捕获机制，保护斑点鲈（Micropterus salmoides）免受海洋水生病毒（MSRV）的侵害。

Abstract

Gut dysbiosis increases MSRV susceptibility without affecting intestinal barrier. • S. dysgalactiae supplementation reduces MSRV loads and improves host survival. • MSRV binds to S. dysgalactiae via cell wall glucan and peptidoglycan. • Commensal bacteria physically trap virions to block host cell attachment. Gut microbiota play a pivotal role in modulating viral infections in mammals, but their functional contributions and mechanisms in teleost fish remain largely unexplored. Here, we investigated whether intestinal commensals influence Micropterus salmoides rhabdovirus (MSRV) infection in largemouth bass ( Micropterus salmoides ) and evaluated and characterized the antiviral activity of a candidate commensal isolate. Antibiotic-induced gut microbiota depletion significantly increased host susceptibility to MSRV, without compromising intestinal barrier integrity, indicating that indigenous microbiota confer protection independent of physical barrier function. A gut-derived Streptococcus dysgalactiae strain isolated from healthy bass intestine was administered as a dietary supplement, resulting in successful enrichment, improved survival, reduced viral loads in liver, spleen and intestine, and no detectable intestinal pathology. Mechanistically, we demonstrate that MSRV virions directly bind to bacterial cell wall glucan and peptidoglycan via specific interactions, and this physical sequestration blocks viral attachment and entry into host cells, as evidenced by electron microscopy, ELISA, competitive binding assays, and in vitro infection models. This physical trapping represents a previously unrecognized antiviral strategy that acts upstream of host immunity, complementing the immune system by reducing the initial viral inoculum. Our findings reveal that a gut-derived bacterium can exert direct antiviral activity through virus–bacteria physical interaction, providing a mechanistic basis for the future design of antiviral interventions against rhabdovira