The effect of temperature on white spot disease progression in a crustacean, Pacifastacus leniusculus

• Published in: Developmental and comparative immunology 2018-12, Vol.89, p.7-13
• Main Authors: Korkut, Gül Gizem, Noonin, Chadanat, Söderhäll, Kenneth
• Format: Article
• Language: English
• Subjects: Animal diseases; Animals; Astacoidea - immunology; Astacoidea - physiology; Astacoidea - virology; Cell cycle; Cell Cycle Checkpoints - drug effects; Cell growth; Cell proliferation; Crayfish; Crustacean; Crustaceans; Demecolcine - pharmacology; Disease Progression; DNA Virus Infections - etiology; DNA Virus Infections - veterinary; Fresh Water; Gene Expression; Genes, Viral; Hematopoietic stem cells; Hemocytes - drug effects; Hemocytes - immunology; Hemocytes - virology; Host-Pathogen Interactions - immunology; Host-Pathogen Interactions - physiology; Innate immunity; Low temperature; Metaphase; Mortality; Pacifastacus leniusculus; Serine; Serine protease; Serine Proteases - genetics; Serine proteinase; Stem cell transplantation; Stem cells; Temperature; Temperature effects; Viral Envelope Proteins - genetics; Virus Replication - drug effects; Virus Replication - physiology; Viruses; White spot syndrome; White spot syndrome virus; White spot syndrome virus 1 - genetics; White spot syndrome virus 1 - pathogenicity; White spot syndrome virus 1 - physiology
• ISSN: 0145-305X; 1879-0089; 1879-0089
• DOI: 10.1016/j.dci.2018.07.026

The effects of temperature on the progression of White Spot Disease (WSD) have been studied in the freshwater crayfish Pacifastacus leniusculus. In this study, we aimed to understand the reason for previously observed low mortalities with white spot syndrome virus (WSSV) infected crayfish at low temperatures. The susceptibility of freshwater crayfish to WSSV was studied at different temperatures. The mortality rate at 6 °C was zero, meanwhile the animals kept at 22 °C developed WSD symptoms and died in a few days after WSSV injections, however upon transfer of animals from 6 °C to 22 °C the mortality reached 100% indicating that the virus is not cleared at 6 °C. Moreover, the VP28 expression at 6 °C was significantly lower compared to animals kept at 22 °C. We injected animals with demecolcine, an inhibitor that arrests the cell cycle in metaphase, and observed a delayed mortality. Furthermore, the VP28 expression was found to be lower in these animals receiving both injections with WSSV and demecolcine since cell proliferation was inhibited by demecolcine. We quantified WSSV copy numbers and found that virus entry was blocked at 6 °C, but not in demecolcine treatments. We supported this result by quantifying the expression of a clip domain serine protease (PlcSP) which plays an important role for WSSV binding, and we found that the PlcSP expression was inhibited at 6 °C. Therefore, our hypothesis is that the WSSV needs proliferating cells to replicate, and an optimum temperature to enter the host hematopoietic stem cells successfully. •WSSV infection into P. leniusculus is temperature dependent.•Cell cycle arrest blocks WSSV replication.•A clip domain serine protease (PlcSP) is necessary for WSSV infection.