Investigation of roles of heat shock proteins for multiplication of Betanodavirus

2015 Fiscal Year Final Research Report

• Project/Area Number: 25450274
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Aquatic bioproduction science
• Research Institution: Hiroshima University
• Principal Investigator: Okinaka Yasushi 広島大学, 生物圏科学研究科, 准教授 (80363034)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 魚類ノダウイルス / 熱ショックタンパク質 / 分子シャペロン / 相互作用 / ウイルス増殖 / 遺伝子ノックダウン / 遺伝子の過剰発現

Outline of Final Research Achievements

Betanodaviruses are the causative agents of viral nervous necrosis in cultured marine fish, causing very high mortality and resulting economic loss in aquatic industry. Although the functions of the viral genome and encoded proteins have been characterized extensively, there is barely any information on host factors required for multiplication of these viruses. HSPs comprise a large family of molecular chaperon proteins induced by various stressors. Thermal stress up-regulated some isoforms of HSP70 and HSP90, and facilitated virus multiplication. Virus infection also up-regulated some HSP70 and HSP90 isoforms. Furthermore, overexpression and knockdown experiments on the HSP isoforms revealed that HSP70-1, HSP70-2, HSP70-5, HSP90-α1, HSP90-α2, and HSP90-β played important roles in multiplication of a betanodavirus. These results indicate that some HSP70 and HSP90 isoforms support betanodavirus multiplication, probably by promoting host and/or viral protein production.

Free Research Field

水族病理