神經壞死症病毒(Nervous necrosis virus, NNV)及台灣石斑魚虹彩病毒(Grouper iridovirus of Taiwan, TGIV)是造成養殖石斑苗大量死亡的病因,NNV造成兩吋以下的魚苗大量死亡,而TGIV則造成一吋以上的魚苗陸續死亡,在養殖石斑魚的一至兩吋苗階段,是兩種病毒容易有共感染的階段。本研究目的在探討NNV及TGIV在同時感染或先後感染時NNV對TGIV複製的影響。活體攻毒實驗結果顯示, 以TGIV單獨感染健康的吋苗,10天後的累計死亡率是100%;然而以NNV先攻毒健康的八分苗,15天後的殘活吋苗再進行TGIV攻毒,則10天後的累計死亡率降至28%。以石斑魚鰭細胞株GF-3 當作體外培養系統,在NNV和TGIV同時感染或NNV先感染的情況下,TGIV的力價會比單獨感染時的力價低2~2.25 Log,但NNV力價卻比NNV單獨感染時力價上升0.25~1.25 Log。但單獨感染NNV的GF-3細胞中可以偵測到Mx基因的表現,在單獨感染TGIV的GF-3細胞中則測不到,顯示只有NNV可以誘發GF-3細胞產生干擾素(Interferon, IFN)反應;抗病毒活性試驗結果顯示,NNV所誘發的干擾素對NNV及TGIV都有抗病毒效果,推測NNV所誘發的干擾素反應可能是造成先後感染(dual-infection)實驗中TGIV力價降低的原因之一。另外,TGIV 是DNA 病毒,NNV是正意單股RNA病毒,同時感染及先後感染實驗結果顯示,TGIV的DNA、RNA及蛋白質複製量都比單獨感染時明顯下降,NNV的RNA複製量則比單獨感染時少許上升,推測造成此現象的原因是NNV的核酸比TGIV小很多,故複製效率因此比TGIV快很多,可能因快速耗損寄主細胞的資源,而造成TGIV力價下降。
Nervous necrosis virus (NNV) and grouper iridovirus of Taiwan (TGIV) were two important pathogens of reared groupers. Serious mortality caused by NNV usually occurs among the groupers smaller than 2 inches, and mortality caused by TGIV always occurs among groupers larger than one inch. In nature, NNV and TGIV had been detected within the same host. The aim of this study is to study the interaction between NNV and TGIV during co-infection and dual-infection.The accumulated mortality of grouper larvae with body length of one inch 10 days post TGIV challenge was 100%. If NNV challenged grouper larvae with body size of 0.8 cm first, then TGIV challenged the survivor larvae 15 days post NNV infection, with body length of 4~4.5cm the accumulated mortality of TGIV-infected groupers declined to 28%. Grouper fin cell line GF-3 is susceptible to either NNV or TGIV. During co-infection or dual-infection of NNV and TGIV in GF-3 cells, the titers of progeny TGIV decreased 2-2.25 Log, but the titers of NNV increased 0.25-1.25 Log. In GF-3 cells, only NNV but not TGIV could induce Mx gene expression. The culture supernatant of NNV-infected GF-3 cells being neutralized by NNV-specific antibodies revealed antiviral activity against both viruses.Therefore, NNV infection induced interferon (IFN) response may be one of the reasons for the decline of TGIV replication during co- or dual- infection.Moreover, the levels of DNA, RNA and protein synthesis of TGIV in GF-3 cells during co- or dual-infection with NNV were much lower than the levels during TGIV sole infection.However, the replication efficiency of NNV during co- or durl-infection was similar to that during NNV sole infection. NNV is a positive sence ssRNA virus, and the genome size is much smaller than that of TGIV which is a dsDNA virus.The decline of TGIV replication level during co- or dual-infection was also possible due to the rapid comsumption of host resources by NNV.
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