Department of Aquatic Animal Diseases and Control, Heilongjiang River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Key Laboratory of Aquatic Animal Diseases and Immune Technology of Heilongjiang Province, Harbin, 150070, China; State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, 430072, China; Pearl River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Key Laboratory of Fishery Drug Development, Ministry of Agriculture and Rural Affairs, Key Laboratory of Aquatic Animal Immune Technology, Guangdong Province, Guangzhou, 510380, China.
Department of Aquatic Animal Diseases and Control, Heilongjiang River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Key Laboratory of Aquatic Animal Diseases and Immune Technology of Heilongjiang Province, Harbin, 150070, China.
Fish Shellfish Immunol. 2020 Jul;102:361-367. doi: 10.1016/j.fsi.2020.05.010. Epub 2020 May 6.
Salmonids can be co-infected by infectious hematopoietic necrosis virus (IHNV) and infectious pancreatic necrosis virus (IPNV) under natural or experimental conditions. To reveal the influence of IPNV on IHNV in co-infections, CHSE-214 cells were inoculated with IPNV at different time intervals prior to or after IHNV infection. Propagation of IHNV was determined by an immunofluorescence antibody test, real-time quantitative polymerase chain reaction, flow cytometry, and virus titration. The results showed that when cells were inoculated with IPNV prior to IHNV, IHNV multiplication was inhibited. This inhibitory effect became stronger with increasing time intervals (P < 0.05). When cells were inoculated with IPNV after IHNV, the inhibitory effect became weaker with increasing time intervals (P < 0.05), and no significant inhibition was observed at 12 h (P > 0.05) compared with the single IHNV infection group. The findings suggest that IHNV is inhibited at the early stage of infection by IPNV and in a time dependent manner during co-infection. Furthermore, the effect of IPNV on IHNV entry and expression of IHNV entry-related genes clathrin, dynamin-2, adaptor protein 2, and vacuolar protein sorting 35 were also determined. The results showed that IPNV did not affect the amount of IHNV entering the cells. However, the expression levels of clathrin and dynamin-2 were significantly lower in co-infection than those in single IHNV infection, which suggests that IPNV likely inhibits IHNV by affecting IHNV invasion via downregulating IHNV entry-related genes clathrin and dynamin-2.
在自然或实验条件下，鲑鱼可以同时感染传染性造血坏死病毒（IHNV）和传染性胰腺坏死病毒（IPNV）。为了揭示 IPNV 在合并感染中的对 IHNV 的影响，将 CHSE-214 细胞在感染 IHNV 之前或之后以不同的时间间隔用 IPNV 接种。通过免疫荧光抗体试验、实时定量聚合酶链反应、流式细胞术和病毒滴定来确定 IHNV 的增殖。结果表明，当细胞先接种 IPNV 后再接种 IHNV 时，IHNV 的增殖受到抑制。这种抑制作用随着时间间隔的增加而增强（P<0.05）。当细胞先接种 IHNV 后再接种 IPNV 时，随着时间间隔的增加，抑制作用变弱（P<0.05），与单独感染 IHNV 组相比，在 12 小时时没有观察到明显的抑制（P>0.05）。研究结果表明，在合并感染中，IPNV 在 IHNV 感染的早期阶段以时间依赖的方式抑制 IHNV。此外，还确定了 IPNV 对 IHNV 进入和 IHNV 进入相关基因网格蛋白、动力蛋白-2、衔接蛋白 2 和液泡蛋白分选 35 表达的影响。结果表明，IPNV 不影响 IHNV 进入细胞的数量。然而，在合并感染中，网格蛋白和动力蛋白-2的表达水平明显低于单独感染 IHNV，这表明 IPNV 可能通过下调 IHNV 进入相关基因网格蛋白和动力蛋白-2来影响 IHNV 的入侵，从而抑制 IHNV。
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