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Baculovirus antiapoptotic protein P35 regulated the host apoptosis to enhance virus multiplication

Yanyan Miao1, Aihua Liang1, Yuejun Fu2

  • 1Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Institute of Biotechnology, Shanxi University, Taiyuan, 030006, People's Republic of China.

Molecular and Cellular Biochemistry
|September 16, 2016
PubMed

Insights

The baculovirus P35 protein (Autographa californica multiple nucleopolyhedrovirus P35) delays apoptosis and enhances virus production. This study reveals P35

Area of Science:

  • Molecular Virology
  • Insect Pathology
  • Cellular Biology

Background:

  • Autographa californica multiple nucleopolyhedrovirus (AcMNPV) encodes the P35 protein, an inhibitor of apoptosis.
  • Previous research indicated that deleting the p35 gene leads to premature cell lysis and reduced virus yield.

Purpose of the Study:

  • To investigate the role of AcMNPV P35 in regulating AcMNPV inhibitor of apoptosis proteins (Ac-IAPs) and Sf9 cell apoptosis protein SfP53.
  • To determine the effect of P35 on progeny virus production.

Main Methods:

  • Overexpression of P35 in AcMNPV-infected Sf9 cells.
  • Analysis of SfP53 and Ac-IAP (iap1, iap2) gene transcription levels.
  • Quantification of progeny virus production.

Main Results:

  • Overexpression of P35 delayed the increase of SfP53 levels and significantly enhanced Ac-IAP gene transcription, particularly iap1, between 24-72 hours post-infection.
  • P35 positively influenced the production of progeny virus.

Conclusions:

  • This study elucidates the intricate relationship between p35, iap1, iap2, SfP53, and AcMNPV replication.
  • Findings provide a theoretical and technological foundation for enhancing the insecticidal efficacy of recombinant AcMNPV.
Keywords:
Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV)Inhibitor of apoptosis geneVirus replicationp35 gene

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