TEMPERATURE ON DIV1 INFECTION IN MACROBRACHIUM ROSENBERGII AND TRANSCRIPTOMIC ANALYSIS

To investigate the effect and regulatory mechanism of temperature on Macrobrachium rosenbergii infected with Decapod iridescent virus 1 (DIV1), we set up five experimental groups at different temperatures (26, 28, 30, 32, and 34℃) for artificial DIV1 infection in this study, and calculated its survival rate. The results showed that the temperature of 34℃ significantly inhibited virus replication in M. rosenbergii, decreased mortality, and extended survival duration. The viral load in the hepatopancreas, gill, and muscle of M. rosenbergii infected with DIV1 was determined at 24h and 72h. The results found that the virus rapidly proliferated within 72hours, however, a notable reduction in the viral load decreased significantly when the water temperature increased to 30℃ or above. In addition, transcriptomic analysis was conducted on hepatopancreas of M. rosenbergii infected with DIV1 at different temperatures, and a total of 8483 differentially expressed genes were identified. Enrichment analysis revealed that these differentially expressed genes were mainly enriched in Arachidonic acid metabolism, Glycolysis/Gluconeogenesis, alpha-Linolenic acid metabolism and other metabolic pathways related to Warburg effect. It is speculated that these pathways and genes may be closely related to the mechanism of viral infection. Furthermore, the expression levels of immune genes CAT, Cu/ZnSOD, CTL, and ACP in M. rosenbergii infected with DIV1, revealing significantly higher expression at temperature of 32℃ compared to other temperatures. This indicates that high temperature can promote an increase in immune gene expression in M. rosenbergii to resist virus invasion. This study provides a comprehensive analysis of the temperature effects on DIV1 infection in M. rosenbergii, elucidating the effects and regulatory mechanism of temperature on virus replication. These findings lay a foundation for further exploration into the molecular mechanism of virus infection and the development of antiviral immune technology.