Abstract
Fish iridoviruses cause systemic diseases with high mortality in various species of wild and farm-raised fish, resulting in severe economic losses. In 1998, we isolated a new epizootic iridovirus in cultured grouper (Epinephelus sp.) in Taiwan, thus named as grouper iridovirus of Taiwan (TGIV). We report here the cloning of TGIV major capsid protein (MCP). Phylogenetic analysis of the iridoviral MCPs confirmed the classification of TGIV into the Megalocytivirus genus. Recombinant TGIV MCP and GIV MCP were then generated to produce polyclonal antibodies. Western blot analysis revealed that the two antisera were species-specific, indicating no common epitope shared by the MCPs of the two viruses. We further assayed the potency of a subunit vaccine containing recombinant TGIV MCP. The vaccine effectively protected grouper from TGIV infection. The result demonstrated that MCP is a suitable antigen for anti-TGIV vaccines.
Highlights
Grouper (Epinephelus coioides) is a commercially important culture species in many Asian countries
The results suggest that there is likely no common epitope shared by the major capsid protein (MCP) of grouper iridovirus (GIV) and TGIV
We reported the cloning of TGIV MCP gene
Summary
Grouper (Epinephelus coioides) is a commercially important culture species in many Asian countries. Viral diseases are a major cause to the decline of grouper fry production. Iridoviruses have been reported to cause severe infection in various stages of the life cycle of grouper. Ranaviruseses that are known to infect marine fish include Singapore grouper iridovirus (SGIV) [5] and grouper iridovirus (GIV) [6]. Megalocytiviruses that infect marine fish include red seabream iridovirus (RSIV) [3,7], sleepy grouper disease iridovirus (GSDIV) [8], and infectious spleen and kidney necrosis virus (ISKNV) [9,10,11]. TGIV could cause up to 60% mortality in the infected grouper fry. Of a recombinant MCP subunit vaccine against TGIV infection in grouper. The p2.G2.SE-x2p1reas-sTioGn aInVd-MPuCrifPicaptiornokofaRreycoomtibcineanxtpTrGeIsVs-iMonCPvaencdtGoIrVw-MaCsPefomr Pprloodyucetdiontoof express recombinant His–GST–PToGlyIcVlon–aMl ACnPtib–oHdieiss and His–GST–GIV–MCP–His proteins. Spleen tissue samples were collected at the appearance of typical clinical symptoms and were subjected to
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