Effect of white spot syndrome virus (WSSV) infection on immune enzyme activity and ultrastructure in the haemolymph tissue of Cherax quadricarinatus (Decapoda, Astacidea)

Crustaceana ◽  
2016 ◽  
Vol 89 (6-7) ◽  
pp. 669-684
Author(s):  
J. J. Ning ◽  
M. M. Zhang ◽  
Q. Q. Tong ◽  
X. Cao ◽  
D. L. Wang ◽  
...  
Keyword(s):  
Enzyme Activities ◽  
White Spot Syndrome Virus ◽  
White Spot ◽  
Immune Protection ◽  
Cell Nuclei ◽  
Cherax Quadricarinatus ◽  
Deformation And Fracture ◽  
Before And After ◽  
Protection Rate ◽  
White Spot Syndrome

To explore the pathogenic mechanism of white spot syndrome virus (WSSV) in crayfish (Cherax quadricarinatus), we analysed activities of the three immune-related enzymes PO, SOD and LSZ in haemolymph tissue ofC. quadricarinatusbefore and after infection, and simultaneously studied the ultrastructural pathology. The results show that WSSV infection affects activities of the three enzymes. After 6-24 h of WSSV infection, the activities of PO, SOD and LSZ increased, but decreased significantly during longer infection times. The enzyme activities in WSSV-infected crayfish were significantly lower than those in controls at 72 h, except for LSZ (). Interestingly, the activities of PO, SOD and LSZ in the group treated with immune-polysaccharides before challenge with WSSV were higher than in the directly infected group, and the immune protection rate reached 51.9%, suggesting that the polysaccharides could improve enzyme activities and enhance antiviral defences of the organism. Ultrastructural pathological changes showed damaged haemolymph tissue, deformed golgiosomes, fuzzy damage in the mitochondrial structures, and nuclear membrane deformation and fracture. High levels of heterochromatin appeared in the nucleus; organoid and chromatin dissolved in dying blood cells, cytoplasm appeared oedematous and cells dissolved. WSSV particles were visible in blood cell nuclei of infected crayfish.

scholarly journals White Spot Syndrome Virus Benefits from Endosomal Trafficking, Substantially Facilitated by a Valosin-Containing Protein, To Escape Autophagic Elimination and Propagate in the Crustacean Cherax quadricarinatus

2020 ◽  
Vol 94 (24) ◽  
Author(s):  
Chuang Meng ◽  
Ling-Ke Liu ◽  
Dong-Li Li ◽  
Rui-Lin Gao ◽  
Wei-Wei Fan ◽  
...  
Keyword(s):  
Delivery System ◽  
Brackish Water ◽  
Viral Genome ◽  
White Spot Syndrome Virus ◽  
Viral Disease ◽  
White Spot ◽  
Acidic Ph ◽  
Cherax Quadricarinatus ◽  
Content Type ◽  
White Spot Syndrome

ABSTRACT As the most severely lethal viral pathogen for crustaceans in both brackish water and freshwater, white spot syndrome virus (WSSV) has a mechanism of infection that remains largely unknown, which profoundly limits the control of WSSV disease. By using a hematopoietic tissue (Hpt) stem cell culture from the red claw crayfish Cherax quadricarinatus suitable for WSSV propagation in vitro, the intracellular trafficking of live WSSV, in which the acidic-pH-dependent endosomal environment was a prerequisite for WSSV fusion, was determined for the first time via live-cell imaging. When the acidic pH within the endosome was alkalized by chemicals, the intracellular WSSV virions were detained in dysfunctional endosomes, resulting in appreciable blocking of the viral infection. Furthermore, disrupted valosin-containing protein (C. quadricarinatus VCP [CqVCP]) activity resulted in considerable aggregation of endocytic WSSV virions in the disordered endosomes, which subsequently recruited autophagosomes, likely by binding to CqGABARAP via CqVCP, to eliminate the aggregated virions within the dysfunctional endosomes. Importantly, both autophagic sorting and the degradation of intracellular WSSV virions were clearly enhanced in Hpt cells with increased autophagic activity, demonstrating that autophagy played a defensive role against WSSV infection. Intriguingly, most of the endocytic WSSV virions were directed to the endosomal delivery system facilitated by CqVCP activity so that they avoided autophagy degradation and successfully delivered the viral genome into Hpt cell nuclei, which was followed by the propagation of progeny virions. These findings will benefit anti-WSSV target design against the most severe viral disease currently affecting farmed crustaceans. IMPORTANCE White spot disease is currently the most devastating viral disease in farmed crustaceans, such as shrimp and crayfish, and has resulted in a severe ecological problem for both brackish water and freshwater aquaculture areas worldwide. Efficient antiviral control of WSSV disease is still lacking due to our limited knowledge of its pathogenesis. Importantly, research on the WSSV infection mechanism is also quite meaningful for the elucidation of viral pathogenesis and virus-host coevolution, as WSSV is one of the largest animal viruses, in terms of genome size, that infects only crustaceans. Here, we found that most of the endocytic WSSV virions were directed to the endosomal delivery system, strongly facilitated by CqVCP, so that they avoided autophagic degradation and successfully delivered the viral genome into the Hpt cell nucleus for propagation. Our data point to a virus-sorting model that might also explain the escape of other enveloped DNA viruses.

A barrier-to-autointegration factor promotes white spot syndrome virus infection in a crustacean Cherax quadricarinatus

2020 ◽  
Vol 105 ◽  
pp. 244-252 ◽  
Author(s):  
Ling-ke Liu ◽  
Yan Gao ◽  
Rui-lin Gao ◽  
Dong-li Li ◽  
Qiu-xia Zhang ◽  
...  
Keyword(s):  
Virus Infection ◽  
White Spot Syndrome Virus ◽  
White Spot ◽  
Cherax Quadricarinatus ◽  
White Spot Syndrome

scholarly journals Lipid of white-spot syndrome virus originating from host-cell nuclei

2008 ◽  
Vol 89 (11) ◽  
pp. 2909-2914 ◽  
Author(s):  
Qing Zhou ◽  
Hui Li ◽  
Yi-Peng Qi ◽  
Feng Yang
Keyword(s):  
Neutral Lipid ◽  
Host Cell ◽  
High Performance ◽  
White Spot Syndrome Virus ◽  
Procambarus Clarkii ◽  
White Spot ◽  
Gas Chromatography Mass Spectrometry ◽  
Cell Nuclei ◽  
White Spot Syndrome ◽  
Layer Chromatography

The hypothesis that white-spot syndrome virus (WSSV) generates its envelope in the nucleoplasm is based on electron microscopy observations; however, as yet there is no direct evidence for this. In the present study, the lipids of WSSV and the nuclei of its host, the crayfish Procambarus clarkii, were extracted and the neutral lipid and phospholipid contents were analysed by high-performance liquid chromatography, thin-layer chromatography and gas chromatography/mass spectrometry. Phosphatidylcholine (PC) and phosphatidylethanolamine comprised 62.9 and 25.8 %, respectively, of WSSV phospholipids, whereas they comprised 58.5 and 30 %, respectively, of crayfish nuclei phospholipids. These two phospholipids were the dominant phospholipids, and amounts of other phospholipids were very low in the total WSSV and crayfish nuclei phospholipids. The data indicate that the phospholipid profile of WSSV and crayfish nuclei are similar, which is in agreement with the model that the lipids of WSSV are from the host-cell nuclei. However, the fatty acid chains of PC were different between the WSSV virions and crayfish nuclei, and the viral neutral lipid component was also found to be somewhat more complicated than that of the host nuclei. The number of species of cholesterol and hydrocarbon in virus neutral lipid was increased compared with that in host-cell nuclei neutral lipid. It is suggested that the differences between WSSV and its host are either due to selective sequestration of lipids or reflect the fact that the lipid metabolism of the host is changed by WSSV infection.

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