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AcMNPV-BmK IT improves the progeny virus production via baculovirus GP64 envelope fusion protein
Yuejun Fu1, Yanyan Miao2, Shuhua Zheng3
1Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Institute of Biotechnology, Shanxi University, Taiyuan, 030006, People's Republic of China. yjfu@sxu.edu.cn.
Objectives:
To analyze the mechanisms underlying the impact of recombinant Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV)-mediated BmK IT expression on the function of baculovirus GP64 envelope fusion protein and progeny virus production.
Results:
Viral propagation assay indicated that overexpression GP64 could promote replication of AcMNPV. AcMNPV-mediated expression of BmK IT also promoted replication of AcMNPV. Immunofluorescence analysis showed BmK IT, which was regulated by very early promoter IE1 in AcMNPV, could make the GP64 protein move to the cytomembrane soon after transfection. BmK IT, which is regulated by P10 protein promoter (P10) and polyhedrosis promoter (PH), could promote the expression of GP64.
Conclusion:
BmK IT, regulated by very early promoter IE1, P10 protein promoter (P10) and PH, accelerated the expression of GP64 protein, promoted its early cytomembrane localization and then triggered virus budding and progeny virus production.
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