Study of the crosstalk between heat shock response and autophagy under NNV infection in groupers

Abstract

The outbreak of nervous necrosis virus (NNV) has been the major problem that causes high mortality in groupers Under NNV induced stress the balance of homeostasis is disrupted and proteins become dysfunctional In order to maintain host homeostasis there are two main protein quality control in eukaryotes: heat shock response (HSR) and autophagy However it still remains unknown how groupers mediate two homeostatic responses during viral infection In this study HSF1 and LC3 are used as markers to determine the interaction between both responses Through gain and loss of function experiments HSR controlled autophagy but sufficient autophagy was negatively fed back to HSR showing that HSR and autophagy regulated each other Under stress of NNV infection heat shock (36°C) or overexpression of HSF1b promoted NNV replication with higher viral RNA2 expression but rapamycin treatment or overexpression of LC3 reduced the viral load indicating that two responses had opposite roles against NNV infection On the other hand the interaction between HSR and autophagy counteracted the degree of NNV CP expression suggesting that the severity of an infection depended on the balance of these two responses Taken together HSR inhibition combined with autophagy activation may provide better protection against NNV infection These findings also help us understand the coordination between the defense mechanisms to improve the grouper survival and reduce the economic loss

Date of Award	2021
Original language	English
Supervisor	Tzong-Yueh Chen (Supervisor)