Epigallocatechin‐3‐gallate inhibits replication of white spot syndrome virus in the freshwater crayfish Procambarus clarkii

2021 ◽  
Author(s):  
Yitong Zhang ◽  
Jinxuan Wen ◽  
Yao Xu ◽  
Hao Wang ◽  
Liqun Lu ◽  
...  
Keyword(s):  
White Spot Syndrome Virus ◽  
Procambarus Clarkii ◽  
White Spot ◽  
Freshwater Crayfish ◽  
White Spot Syndrome

Diagnosis of co-infection with white spot syndrome virus and Aeromonas veronii in red swamp crayfish Procambarus clarkii

Aquaculture ◽  
2021 ◽  
Vol 532 ◽  
pp. 736010
Author(s):  
Gaoliang Yuan ◽  
Lei Zhu ◽  
Xinyu Jiang ◽  
Jie Zhang ◽  
Chao Pei ◽  
...  
Keyword(s):  
White Spot Syndrome Virus ◽  
Procambarus Clarkii ◽  
White Spot ◽  
Aeromonas Veronii ◽  
Red Swamp Crayfish ◽  
White Spot Syndrome

scholarly journals A gC1qR Prevents White Spot Syndrome Virus Replication in the Freshwater Crayfish Pacifastacus leniusculus

2010 ◽  
Vol 84 (20) ◽  
pp. 10844-10851 ◽  
Author(s):  
Apiruck Watthanasurorot ◽  
Pikul Jiravanichpaisal ◽  
Irene Söderhäll ◽  
Kenneth Söderhäll
Keyword(s):  
Cell Culture ◽  
Viral Replication ◽  
White Spot Syndrome Virus ◽  
Pacifastacus Leniusculus ◽  
White Spot ◽  
Tissue Cell ◽  
Freshwater Crayfish ◽  
White Spot Syndrome

ABSTRACT The gC1qR/p32 protein is a multiple receptor for several proteins and pathogens. We cloned a gC1qR homologue in a crustacean, Pacifastacus leniusculus, and analyzed the expression of P. leniusculus C1qR (PlgC1qR) in various tissues. The gC1qR/p32 transcript was significantly enhanced by white spot syndrome virus (WSSV) infection 6 h after viral infection both in vitro in a hematopoietic tissue cell culture (Hpt) and in vivo compared to appropriate controls. Moreover, PlgC1qR silencing in both the Hpt cell culture and live crayfish enhanced the WSSV replication. In addition, by making a recombinant PlgC1qR protein we could show that if this recombinant protein was injected in a crayfish, Pacifastacus leniusculus, followed by injection of WSSV, this significantly reduced viral replication in vivo. Furthermore, if the recombinant PlgC1qR was incubated with Hpt cells and then WSSV was added, this also reduced viral replication. These experiments clearly demonstrate that recombinant PlgC1qR reduce WSSV replication both in vivo and in vitro. The results from a far-Western overlay and glutathione S-transferase pull-down assays showed that PlgC1qR could bind to VP15, VP26, and VP28. Altogether, these results demonstrate a role for PlgC1qR in antiviral activity against WSSV.

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