Abstract
The role of oxidative stress in the pathogenesis of RNA nervous necrosis virus infection is still unknown. Red-spotted grouper nervous necrosis virus (RGNNV) induced free radical species (ROS) production at 12–24 h post-infection (pi; early replication stage) in fish GF-1 cells, and then at middle replication stage (24–48 h pi), this ROS signal may upregulate some expressions of the anti-oxidant enzymes Cu/Zn SOD and catalase, and eventually expression of the transcription factor Nrf2. Furthermore, both antioxidants diphenyliodonium and N-acetylcysteine or overexpression of zebrafish catalase in GF-1 cells also reduced ROS production and protected cells for enhancing host survival rate due to RGNNV infection.Furthermore, localization of ROS production using esterase activity and Mitotracker staining assays found that the ROS generated can affect mitochondrial morphology changes and causes ΔΨ loss, both of which can be reversed by antioxidant treatment. Taken together, our data suggest that RGNNV induced oxidative stress response for playing dual role that can initiate the host oxidative stress defense system to upregulate expression of antioxidant enzymes and induces cell death via disrupting the mitochondrial morphology and inducing ΔΨ loss, which can be reversed by anti-oxidants and zfcatalase, which provide new insight into betanodavirus-induced ROS-mediated pathogenesis.
Highlights
The Nodaviridae family of viruses contains two genera: betanodaviruses, which predominantly infect fish, and alpha-nodaviruses, which mostly infect insects [1,2,3,4,5]
Our data suggest that Red-spotted grouper nervous necrosis virus (RGNNV) induced oxidative stress response for playing dual role that can initiate the host oxidative stress defense system to upregulate expression of antioxidant enzymes and induces cell death via disrupting the mitochondrial morphology and inducing DY loss, which can be reversed by anti-oxidants and zfcatalase, which provide new insight into betanodavirus-induced reactive oxygen species (ROS)-mediated pathogenesis
We found that RGNNV can induce ROS production, causing mitochondrial fragmentation that culminates in host cell death
Summary
The Nodaviridae family of viruses contains two genera: betanodaviruses, which predominantly infect fish, and alpha-nodaviruses, which mostly infect insects [1,2,3,4,5]. Beta-nodaviruses are the causative agents for viral nervous necrosis (VNN), an infectious neuropathological condition characterized by necrosis of the central nervous system, including the brain and retina. VNN can cause massive dying off the larvae and juvenile populations of several marine teleost species [6], and the disease manifestations of these viruses may correlate with modulation of innate or acquired immunity [4,7]. Beta-nodaviruses may prove useful as a model for understanding RNA virus-mediated pathogenesis and disease. RNA1 encodes an
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