Journal
ISCIENCE
Volume 23, Issue 1, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2019.100752
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Funding
- National Key Research and Development Program of China [2018YFD0900605/2]
- Science and Technology Planning Project of Guangdong Province [2018B020204001]
- National Natural Science Foundation of China [31772883]
- Guangdong Natural Science Funds for Distinguished Young Scholars [2016A030306041]
- Tip-top Scientific and Technical Innovative Youth Talents of Guangdong special support program [2016TQ03N504]
- Fundamental Research Funds for the Central Universities [17lgpy62]
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Viruses need to hijack and manipulate host proteins to guarantee their replication. Herein, we uncovered that the DNA virus white spot syndrome virus (WSSV) established a novel positive feedback loop by hijacking the host JNK pathway via its immediate-early 1 (IE1) protein to drive replication. Specifically, the WSSV IE1 bound to host JNK, and enhanced JNK autoactivation by autophosphorylation, and in turn, elevated JNK kinase activity to its substrate c-Jun and induced IE1, which resulted in a viral gene-mediated positive feedback loop. Moreover, the activation of this loop is able to induce wsv056, wsv249, and wsv403, in addition to IE1 itself. Disruption of this loop during WSSV infection by knockdown of JNK, c-Jun or IE1 led to an increased survival rate and lower viral burdens in shrimp. Taken together, this loop may provide a potential target for the development of specific antiviral strategies or agents against WSSV infection.
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