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Acta tropica · 2026

Natural periocular infection by Kudoa bora in Osteomugil perusii: a case study with transcriptomic evidence of immune suppression and impaired visual pathways.

СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Li Xiaolu, Tan Xiaoping, Zhao Yuanjun, Chen Xue, Xiong Yalin, Yang Chengzhong

Аннотация

Kudoa bora (Fujita, 1930) is a myxosporean parasite primarily infecting the skeletal muscle of mugilid fishes. In this study, we report for the first time that K. bora can infect the periocular tissues of Osteomugil perusii (Valenciennes, 1836). A comparative transcriptomic approach was employed to preliminarily characterize the molecular responses of the host's periocular tissues to the parasitic infection. A total of 2,954 differentially expressed genes (DEGs) were identified between the infected and uninfected groups, of which 1,305 were upregulated and 1,649 were downregulated. Enrichment analysis of the DEGs revealed that metabolic pathways such as ribosome biogenesis, oxidative phosphorylation, and DNA repair were significantly upregulated, suggesting that the host may activate protein translation and energy compensation mechanisms under stress induced by K. bora infection. In contrast, the cytokine-cytokine receptor interaction and TGF-β signaling pathways were markedly downregulated, suggesting that periocular infection may be associated with a certain degree of local immune suppression. Widespread downregulation of genes involved in eye morphogenesis, lens structural proteins, and visual signal transduction was observed, potentially compromising visual function. Collectively, periocular infection by K. bora may compromise host visual function through the combined suppression of immune pathways and vision-related gene expression. This study extends the known parasitic site of K. bora and provides preliminary molecular evidence for pathogenic mechanisms of myxosporean infection in fish periocular tissues.

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

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