Journal
AQUACULTURE
Volume 530, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.aquaculture.2020.735932
Keywords
Antennal gland; WSSV; Invasion route; Salinity stress; Litopenaeus vannamei
Categories
Funding
- National Natural Science Foundation of China [31902407]
- Key Program of National Natural Science Foundation of China [31830100]
- China Agriculture Research System-48 [CARS-48]
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This study confirmed that the antennal gland is an entry point for WSSV infection in shrimp, and also found that salinity stress can accelerate WSSV replication in the antennal gland and the progression of the disease.
White spot syndrome virus (WSSV) is an extremely destructive virus in shrimp farming which has caused a serious economic loss to global shrimp industry. Learning its infection routes is the basis for WSSV prevention and control. The digestive tract and gill were generally considered to be the target tissues for WSSV entry into shrimp. However, whether there is any other target tissue for WSSV entry into the shrimp is still not clear. In the present study, we firstly found that the transcripts of WSSV could be detected in the antennal gland of the Pacific white shrimp Litopenaeus vannamei cultured in the sea water without any signs of disease. Considering that the antennal gland is an important organ which functions in regulating the osmotic pressure and balance of ions in shrimp, we want to know whether it is also an entry for WSSV infection to shrimp. The spatial expressions of WSSV in shrimp tissues including antennal gland were firstly analyzed in shrimp naturally infected with WSSV, and the data showed that WSSV could be detected in antennal gland of shrimp at the early stages of WSSV infection, and intact virus particles were observed under transmission electronic microscope. Reverse perfusion of WSSV into antennal gland could cause the infection and lead to the death of shrimp. Incubation of WSSV with antennal gland tissues in vitro also led to the replication of WSSV in cultured antennal gland. These data indicated that antennal gland was an entry of WSSV into shrimp to cause the infection. The effect of salinity on WSSV infection was analyzed, and the data showed that salinity stress could induce faster WSSV replication in antennal gland, and accelerate the process of disease. Our study confirmed a new infection route of WSSV, and salinity stress could lead to the disease outbreak caused by WSSV. These data will provide useful information for the development of strategy for WSSV prevention and control.
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