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Transcriptional profile of pyruvate kinase and pancreatic lipase encoding mRNA s of the Pacific whiteleg shrimp Penaeus vannamei during Pst DV ‐1 infection
Author(s) -
OlguínLeón Patricia,
EnríquezEspinoza Tania,
MendozaCano Fernando,
EncinasGarcía Trinidad,
SánchezPaz Arturo
Publication year - 2017
Publication title -
aquaculture research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.646
H-Index - 89
eISSN - 1365-2109
pISSN - 1355-557X
DOI - 10.1111/are.13380
Subject(s) - biology , pyruvate kinase , shrimp , penaeus , lipase , hatchery , gene , glycerol kinase , penaeidae , kinase , microbiology and biotechnology , biochemistry , zoology , metabolism , glycolysis , ecology , fishery , enzyme , crustacean , decapoda , fish <actinopterygii>
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 (Pst DV ‐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 Pst DV ‐1 induces metabolic reprogramming of P. vannamei to achieve a successful replication. In this study, the effects of Pst DV ‐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 Pst DV ‐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 mRNA s offers initial clues on the potential metabolic alteration that contribute to Pst DV ‐1 pathogenesis.