The innate antiviral response through the RIG-1-like receptor pathway is oriented towards a key regulatory molecule, mitochondrial antiviral signaling protein (MAVS). Localized to the mitochondria, MAVS coordinates the interferons (IFN) production through regulated signaling cascades. Protein-protein interaction, post-translational modifications, and mitochondrial dynamics considerably regulate MAVS signaling on the mitochondrial membrane. This review gives insight into the inevitable role of MAVS in the innate antiviral immune response of fish.
The mandarin fish ranavirus (MRV), classified within the genus Ranavirus of the Iridoviridae family, is a lethal pathogen to Mandarin fish (Siniperca chuatsi). Currently, no approved treatment exists, underscoring the urgent need for therapeutic strategies. In this study, we aimed to investigate the antiviral activity of epigoitrin against MRV. An in vitro antiviral activity assay revealed that the CC50 of epigoitrin is 43.16 μM, as determined by the CCK-8 assay. Epigoitrin effectively reduced the number of MRV copies from 8.63 × 108 copies/mL to 1.82 × 108 copies/mL, exhibiting dose-dependent inhibition of MRV replication. The effective concentration (EC50) of epigoitrin was further determined to be 13.72 μM. Moreover, epigoitrin diminished the MRV-induced cytopathic effect as observed under a light microscope and suppressed the expression of major caspid protein of MRV (MRV-MCP), as visualized by immunofluorescence assay. It was revealed that epigoitrin primarily exerts its antiviral effects during the stage of viral replication. Further investigation into the immune response revealed that epigoitrin significantly upregulated the gene expression of Mx1 (5-fold), IFITM (2.5-fold), viperin (10-fold), ISG15 (15-fold), and IRF5 (2-fold). This suggests that epigoitrin indirectly unleashes its antiviral function by activating the host's interferon (IFN) immune response. In conclusion, our findings indicate that epigoitrin holds great potential as a therapeutic agent against MRV infection by modulating the IFN pathway.
日本の海産魚類養殖におけるLactococcus感染症の原因細菌は血清型および遺伝学的解析によりLactococcus garvieae Ⅰ型,L. formosensis (従来のL. garvieae Ⅱ型) およびL. garvieae Ⅲ型に分類される。各型の判別法として用いられる抗血清によるスライド凝集試験では,複数の抗血清に凝集を示す株の型判別が困難であり,従来のPCRでは,Ⅰ型レンサ球菌とⅢ型レンサ球菌を判別できなかった。本研究では,各型に特異的な遺伝子配列からプライマーを設計し,マルチプレックスPCRによる判別法の開発を試みた。マルチプレックスPCRを実施した結果,各型から予想サイズの増副産物が確認され,海産魚類以外を由来とするLactococcus属細菌からは増副産物は得られなかった。本マルチプレックスPCRは,日本で発生しているレンサ球菌の各型の判別法として有効であることが示された。
Aquaculture of the red seabream Pagrus major predominantly utilizes artificial seedlings of high-growth strains. Although effective broodstock management is crucial for sustainable production, internal parasitism in brood fish, particularly by the gonadal nematode Philometra madai, is often neglected. Despite its common occurrence in adult red seabream gonads, infection status of broodstocks and the effects on the brood fish health remain unexplored. This study conducted a 14-month survey on 3- to 4-year-old brood red seabream. Worm carcasses were consistently found in both male and female gonads throughout the year, with overall average prevalence of 86.4%. In some cases, these carcasses filled the entire gonad, including ovarian cavity and sperm ducts, extending to the area near the cloaca, potentially impeding ovulation and sperm release. However, no significant effects on gonadal development were observed and there was no correlation between worm weight and host weight, condition factor, or gonadosomatic index. Live P. madai were detected only during the red seabream spawning season, from March to May, with their maturation synchronized with host reproduction. This study represents the first survey of P. madai infections in high-growth strain red seabream broodstock.
EIBSの病原体PRV-2 をギンザケ稚魚に実験感染した後,脾臓内のウイルスゲノムコピー数と血清中のELISA抗体価を経時的に測定し,ヘマトクリット値と赤血球封入体の消長との関連を検討した。ヘマトクリット値は感染後に直ちに低下しはじめ,40日目に最低値を示し,その後徐々に回復した。赤血球封入体は感染後20日目から40日目の間にのみ観察され,ウイルスゲノムのコピー数も感染後30日目にピークに達した。一方,ELISA 抗体価は赤血球封入体が見られずヘマトクリット値が回復し始めた感染後60日目に初めて8尾中6尾で弱く上昇し,80日目には全個体で顕著に上昇した。