アクアビルナウイルスによるVNN抵抗性の誘導

非病原性アクアビルナウイルス(ABV)を予め接種され、その 7 日後にベータノダウイルス(NNV)で攻撃されたマハタは NNV 感染に対して強い抵抗性を示した。他方、ヒラメではNNVに対する感受性が低いため死亡率からABVの効果をみることはできなかったが、脳および腎臓におけるNNVの消長をみると、両魚種とも ABV 処理魚において明らかにウイルス感染力価の低下が認められた。この防御は、ABVにより誘導されるインターフェロン関連タンパク質に因ると考えられた。
Experimental dual-infections with a non-lethal aquabirnavirus (ABV) and a lethal betanodavirus (redspotted grouper nervous necrosis virus: RGNNV) were carried out in Japanese flounder Paralichthys olivaceus and sevenband grouper Epinephelus septemfasciatus. In the dual-infection group, ABV was intramuscularly (IM) injected into fish seven days before the IM-injection with RGNNV. In the experiments with flounder, a high expression of an Mx gene, a molecular marker for type I interferon(s) (IFM) production, occurred in the head kidneys and brains at Day 7 post-ABV injection. Although-no mortality was found not only in the dual-infected group but also in the single infection group with RGNNV (control group), the infective titers of RGNNV in the tissues of the dual-infected group were significantly lower at any sampling times than those in the control group. In the experiments with grouper, the preceding ABV infection resulted in complete protection against RGNNV infection. The infective titers of RGNNV in the tissues were also lower in the dual-infected group than in the control group throughout the experiments, and finally the virus disappeared from the head kidneys and brains of the dual-infected group at Day 14 and Day 56 postinjections, respectively. These results suggest that an ABV-induced IFN(s) effectively suppresses the progression of secondary betanodavirus infection.