Establishment of infection mode and Penaeus monodon hemocytes transcriptomics analysis under decapod iridescent virus 1 (DIV1) challenge

With the increasing density of shrimp breeding, environmental deterioration and stress associated with intensification have caused diseases occurred frequently. Due to the high fatality rate of decapod iridescent virus 1 (DIV1), a new type of virus discovered in shrimp in recent years, it has caused serious damage to the shrimp farming industry. Penaeus monodon is one of the commonly cultivated species of prawns in the world. In the current study, LD50 was calculated to evaluate the virulence of DIV1 and the DIV1 copies in five tissues were quantitatively detected, which proved that P. monodon could be a host of DIV1. On these basis, a stable and effective DIV1 infection (including latent infection and acute infection) model was established for the first time. In addition, RNA-Seq platform and bioinformatics analysis were used to investigate the hemocyte immune response to DIV1 infection in P. monodon. A total of 31,657 unigenes were find significant assembled when compared to known sequences in major databases, and a total of 29,820 SSRs were obtained in the hemocytes transcriptome. A total of 6236 differentially expressed genes (DEGs) were identified, including 3140 upregulated genes and 3096 down-regulated genes. Through the KEGG pathway enrichment analysis of DEGs, six immune-related pathways were enriched significantly, including Toll and Imd signaling pathway, PI3K-Akt signaling pathway, NF-kappa B signaling pathway, NOD-like receptor signaling pathway, Lysosome and MAPK signaling pathway. Moreover, many DEGs associated with Cholesterol metabolism, Pyruvate metabolism, Arginine and proline metabolism, Nicotinate and nicotinamide metabolism, Pyrimidine metabolism, Tyrosine metabolism and Alanine, aspartate and glutamate metabolism were also significantly modified. Moreover, Glycolysis / Gluconeogenesis and Pentose phosphate pathway, as the markers of Warburg effect, were significantly up-regulated after DIV1 infection. This study provides an ideal infection model for studying the molecular mechanism of P. monodon from the latent infection stage to the acute infection stage, initially reveals the molecular mechanism of DIV1 infection in P. monodon and provides valuable genetic resources and research methods for following molecular marker development and screening the families of P. monodon resistant to DIV1. The ultimate goal is to develop methods to avoid disease outbreaks in farmed shrimp.