Interference of the replication of grouper iridovirus by grouper nervous necrosis virus during co- and dual- infection

碩士 === 國立臺灣大學 === 動物學研究研究所 === 94 === 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 groupe...

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Bibliographic Details
Main Authors: Fu-Chih Hsu, 許富智
Other Authors: Shau-Chi Chi
Format: Others
Language:zh-TW
Published: 2006
Online Access:http://ndltd.ncl.edu.tw/handle/01118287121562890373
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Summary:碩士 === 國立臺灣大學 === 動物學研究研究所 === 94 === 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.