ArticleBMC microbiology2026
Systemic remodeling of the multi-organ virome following Echinococcus infection in mice.
Article in BMC microbiology, 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
The interaction between parasitic infection and the host virome represents a frontier issue in microbial ecology, yet how Echinococcus infection affects the multi-organ virome and whether these alterations hold diagnostic or interventional potential remains poorly understood. In this study, we performed viral metagenomic sequencing on gut, liver, and lung samples from both infected and uninfected mice, integrating community structure clustering, diversity indices, and differential analyses, including STAMP and LEfSe. Our results reveal that Echinococcus infection induced significant tissue-specific virome remodeling. Compared to healthy controls, gut virome diversity increased, characterized by marked expansion of the class Caudoviricetes, particularly the family Siphoviridae (LDA > 4), alongside Picornaviridae enrichment (LDA > 4). In contrast, virome diversity decreased in both the liver and lung, with significant enrichment of Reoviridae (LDA > 4) in the liver and Retroviridae (LDA > 4) in the lung, respectively. Conversely, Picobirnaviridae (LDA > 4) was significantly reduced in the infected liver and lung. Based on phylogenetic analysis, Echinococcus infection significantly altered the murine gut viral community, with eukaryotic viruses (e.g., norovirus, picobirnavirus, and picornavirus) detected exclusively in infected animals, while bacteriophage populations remained stable across groups. Phage host prediction further revealed that phages enriched in infected samples targeted opportunistic pathogens (Clostridium septicum, Trueperella pyogenes), whereas control phages predominantly targeted commensals (Bacteroides thetaiotaomicron). Together, these findings demonstrate that Echinococcus infection drives both eukaryotic virus enrichment and a shift in phage predation toward pathogens, suggesting that infection-induced immune modulation creates a permissive environment for viral replication and associated bacterial dysbiosis.
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