4.7 Article

WSSV latency is maintained by a dynamic balance of host immune factors and disturbed by exposure to bacterial infection and low salinity

期刊

AQUACULTURE
卷 575, 期 -, 页码 -

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ELSEVIER
DOI: 10.1016/j.aquaculture.2023.739747

关键词

Shrimp; White spot syndrome virus (WSSV); Latency; Reactivation

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This study developed a WSSV latency model through low multiplicity infection and found that this method can establish WSSV latency in shrimp. It also discovered that multiple host factors and stimuli can reactivate WSSV latency, including bacterial infection and low salinity stress.
Shrimp is one of the primary aquaculture species worldwide. The white spot syndrome virus (WSSV) is a highly lethal, stress-dependent virus that has led to enormous economic losses in shrimp aquaculture. WSSV can trigger a persistent infection in shrimp (latency), which can be reactivated to become an acute infection following various stimuli. However, the molecular mechanisms underlying the WSSV latency establishment and the induction of reactivation are poorly understood. A WSSV latency model using low multiplicity infection via intramuscular injection was developed in this study. This research examined the effects of multiple host factors and stimuli on WSSV latency. These effects generated latency reactivation in this model. The outcomes revealed that low multiplicity infection via intramuscular injection could be applied to establish WSSV latency in shrimp. Besides, the expression levels of host genes IRF, Dorsal and Relish were found to be substantially correlated with viral loads during WSSV latent infection in vivo. The knockdown of IRF resulted in elevated viral loads and rendered the reactivation of WSSV latency to acute infection that caused mass mortality among shrimp. Furthermore, several bacterial infection and low salinity stress could induce WSSV transitions from latent to acute infection. Noteworthily, the expression levels of Dorsal and Relish, which are considered to promote the replication of WSSV, are upregulated following bacterial infection and low salinity stress. These results indicated that a delicate balance between host and WSSV interaction regulates the latency establishment. This balance could be broken by several stimuli, such as bacterial infection and low salinity stress, which will provide insights into developing management strategies for WSSV prevention and control.

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