The hemolymph melanization response is related to defence against the AcMNPV infection in Bombyx mori

Tao Li1,2, Xueyang Wang1,3, Sheng Qin1,3

  • 1Jiangsu Key Laboratory of Sericultural Biology and Biotechnology, School of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang, Jiangsu, China.

Insights

Silkworm immune defense involves melanization, a process regulated by the prophenoloxidase (proPO) cascade. This study reveals how Autographa californica multiple nucleopolyhedrovirus (AcMNPV) affects melanization in susceptible and resistant silkworm strains.

Area of Science:

  • * Insect immunology
  • * Biochemistry
  • * Molecular biology

Background:

  • * Melanization, crucial for arthropod immunity, is mediated by the prophenoloxidase (proPO) activation cascade.
  • * Previous studies indicated a lack of melanization in the p50 silkworm strain upon Autographa californica multiple nucleopolyhedrovirus (AcMNPV) infection, but the mechanism remained unclear.
  • * Understanding this immune evasion strategy is vital for insect disease management.

Purpose of the Study:

  • * To elucidate the mechanism behind AcMNPV's inhibition of hemolymph melanization in silkworms.
  • * To compare the melanization response in AcMNPV-susceptible (p50) and resistant (C108) silkworm strains.
  • * To investigate the role of proPO system genes in AcMNPV infection.

Main Methods:

  • * Analysis of hemolymph melanization levels in silkworm strains post-AcMNPV inoculation.
  • * Measurement of prophenoloxidase (PO) activity in hemolymph.
  • * Quantitative analysis of BmPPO1, BmPPO2, and BmPPAE gene expression using RT-qPCR.
  • * In vitro assessment of viral activity in the presence of hemolymph melanization.

Main Results:

  • * Resistant C108 strain exhibited higher hemolymph melanization than susceptible p50 strain at late infection stages (72–120 hpi).
  • * PO activity decreased in p50 but increased in C108; BmPPO1 and BmPPO2 expression was downregulated in p50 but unchanged in C108.
  • * BmPPAE gene expression was upregulated in both strains during infection, and melanization reduced viral activity in vitro.

Conclusions:

  • * Silkworm hemolymph melanization is a key defense mechanism against AcMNPV infection.
  • * AcMNPV employs strategies to inhibit melanization in susceptible strains, likely involving downregulation of proPO system components.
  • * The differential regulation of the proPO system in resistant strains highlights its importance in antiviral immunity.