An Anticarsia gemmatalis multiple nucleopolyhedrovirus mutant, vApAg, induces hemocytes apoptosis in vivo and displays reduced infectivity in larvae of Anticarsia gemmatalis (Hübner) (Lepidoptera: Noctuidae)

Virus Res. 2007 Dec;130(1-2):182-92. doi: 10.1016/j.virusres.2007.06.010. Epub 2007 Jul 23.

Abstract

An Anticarsia gemmatalis multiple nucleopolyhedrovirus (AgMNPV) mutant, vApAg, induces apoptosis in a cell culture derived from Anticarsia gemmatalis (UFL-AG-286), reducing viral progeny. We have investigated apoptosis induction in vivo by vApAg in A. gemmatalis larvae and its correlation to infectivity reduction. LC(50), LD(50), LT(50) and the mean time to death of larvae were determined for vApAg and AgMNPV. Apoptosis was accessed for hemocytes of infected larvae using light and transmission electron microscopy. All types of hemocytes can be infected by vApAg. After 12h post-infection (h p.i.), typical cellular modifications associated to nucleopolyhedrovirus infection were observed. Apoptosis becomes evident after 24h p.i., and massive after 72h p.i. Necrosis of infected cells was also observed. Despite cell death, hemocytes produced budded viruses and polyhedra. Pl and gh1-type hemocytes presented phagocytic activity. Agarose gel electrophoresis revealed fragmentation of hemocytes DNA at late times post-infection. The LC(50) and LD(50) were between five- and six-fold higher for vApAg. The LT(50) and the mean time to death were higher for vApAg in a same treatment or for a similar mortality induced by AgMNPV. These results show correlation of apoptosis and the reduced infectivity of vApAg in A. gemmatalis larvae.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Cells, Cultured
  • DNA Fragmentation
  • Hemocytes / cytology
  • Hemocytes / ultrastructure
  • Hemocytes / virology*
  • Larva
  • Lethal Dose 50
  • Microscopy, Electron, Transmission
  • Moths / virology*
  • Mutation
  • Necrosis / virology
  • Nucleopolyhedroviruses / genetics*
  • Nucleopolyhedroviruses / pathogenicity*
  • Survival Analysis
  • Time Factors
  • Virulence / genetics