The regulation of shrimp metabolism by the white spot syndrome virus (WSSV)

For more than three decades, infectious diseases have been one of the major causes of economic losses in the global shrimp industry. One of the deadliest of the shrimp pathogens is white spot syndrome virus (WSSV), which causes mass mortality in farmed shrimp. Various aspects of WSSV pathogenicity have been studied, but in this review, we will focus only on one of them, namely metabolic reprogramming. WSSV's modulation of host metabolism affects glycolysis, the tricarboxylic acid (TCA) cycle, glutaminolysis and lipid metabolism. Several signaling pathways are involved in this regulation, including JAK-STAT, PI3K-AKT-mTOR, MAPK and Ras-Raf-MEK, with the PI3K-Akt-mTOR pathway in particular playing a critical role in activating the WSSV-induced Warburg effect. Taken together, these changes benefit the virus by facilitating WSSV replication. In this review, we summarize current knowledge regarding the metabolism-related aspects of WSSV pathogenesis, and discuss the mechanisms by which this virus reprograms its host's metabolic pathways. A deeper understanding of these pathways, key metabolic enzymes and signaling mechanisms is potentially important for the development of effective anti-WSSV strategies.

Automated summary

For over three decades, infectious diseases have caused significant economic losses in the global shrimp industry, with white spot syndrome virus (WSSV) being one of the deadliest pathogens. WSSV modulates host metabolism by affecting glycolysis, TCA cycle, glutaminolysis, and lipid metabolism, with the PI3K-Akt-mTOR pathway playing a critical role in activating the WSSV-induced Warburg effect. Understanding these metabolic pathways and signaling mechanisms is crucial for developing effective anti-WSSV strategies.