Transcriptional profile of pyruvate kinase and pancreatic lipase encoding mRNAs of the Pacific whiteleg shrimp Penaeus vannamei during PstDV‐1 infection

Beyond their ability to infect and spread, viruses lack the ability to replicate by their own. To counter this, viruses have evolved strategies to exploit the host's machinery for the production of new virions. However, viruses are by no means merely passive consumers of host metabolic products. Viruses induce remarkable changes in their host's cellular metabolism, yielding a metabolic state, to meet its specific requirements. The decapod penstyldensovirus (PstDV-1) is probably the most prevalent virus affecting shrimp farming and has been associated with massive mortality outbreaks in hatchery-reared larvae and juveniles of Penaeus stylirostris, and results in developmental deformities in symptomatic specimens of P. vannamei. Previous studies have suggested that PstDV-1 induces metabolic reprogramming of P. vannamei to achieve a successful replication. In this study, the effects of PstDV-1 infection over the gene expression of pyruvate kinase and pancreatic lipase of the shrimp P. vannamei were evaluated. The expression of both genes was significantly altered by PstDV-1 infection, which may lead to the accumulation of specific metabolites, as lactate and fatty acids, providing a suitable platform for viral assembly and replication. The transcriptional profile of pyruvate kinase and pancreatic lipase-encoding mRNAs offers initial clues on the potential metabolic alteration that contribute to PstDV-1 pathogenesis.