SpBcl2 promotes WSSV infection by suppressing apoptotic activity of hemocytes in mud crab, Scylla paramamosain

Jun 30, 2019Developmental and comparative immunology

SpBcl2 helps WSSV infection by reducing cell death in mud crab immune cells

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Abstract

The expression of SpBcl2 increased at both the transcriptional and post-transcriptional levels after WSSV infection.

WSSV infection is associated with a significant decrease in hemocyte apoptosis in mud crabs.
An increase in cytochrome c levels was observed alongside the upregulation of SpBcl2.
SpBcl2 may suppress apoptosis by preventing the release of cytochrome c from mitochondria.
The findings provide new insights into how mud crabs respond to WSSV infection.

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White spot syndrome virus (WSSV) is one of the most virulent and widespread pathogens that infect almost all marine crustaceans and therefore cause huge economic losses in aquaculture. The Bcl2 protein plays a key role in the mitochondrial apoptosis pathway, which is a crucial immune response in invertebrates. However, the role of Bcl2 in apoptosis and immunoregulation in mud crab, Scylla paramamosain, is poorly understood. Here, the Bcl2 homolog (SpBcl2) in S. paramamosain was cloned and its role in WSSV infection explored. The expression of SpBcl2 increased at both the transcriptional level and post-transcriptional level after WSSV infection, while the hemocytes apoptosis decreased significantly. Furthermore, there was increase in the level of cytochrome c coupled with an upregulation in the expression of SpBcl2. These results indicated that SpBcl2 suppressed apoptosis by preventing the release of cytochrome c from mitochondria, thereby promoting WSSV replication in mud crab. The findings here therefore provide novel insight into the immune response of mud crabs to WSSV infection.

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