Institute of Marine Biology, College of Oceanography, Hohai University, Nanjing, PR China.
National Pathogen Collection Center for Aquatic Animals, Shanghai Ocean University, Shanghai, PR China.
J Gen Virol. 2020 Feb;101(2):145-155. doi: 10.1099/jgv.0.001363.
Elevation of heat-shock protein expression, known as cellular heat-shock responses, occurs during infection of many viruses, which is involved in viral replication through various mechanisms. Herein, transcriptome analysis revealed that over-expression of non-structural protein NS31 of grass carp reovirus (GCRV) in grass carp kidney (CIK) cells specifically induced expression of heat-shock response (HSR) genes and . We further found that, among the HSR genes, only HSP70 protein were shown to be efficiently induced in fish cells following NS31 over-expression or GCRV infection. Employing a luciferase assay, we were able to show that the promoter of the HSP70 gene can be specifically activated by NS31. In addition, over-expressing HSP70 in grass carp CIK cells resulted in enhanced replication efficiency of GCRV, and an inhibitor for HSP70 resulted in the inhibition of GCRV replication, indicating that HSP70 should serve as a pro-viral factor. We also found that NS31 could activate HSP70 expression in cells of other vertebrate animals. Similar inducing effect on HSP70 expression was demonstrated for NS31-homologue proteins of other aquareoviruses including American grass carp reovirus (AGCRV) and GRCV (green river chinook virus). All these results indicated NS31 proteins in the genus should play a key role for up-regulating specific HSP70 gene during viral replication.
