The Autographa californica M nucleopolyhedrovirus fibroblast growth factor accelerates host mortality

Chanitchote Detvisitsakun1, Erica L Cain, A Lorena Passarelli

  • 1Molecular, Cellular, and Developmental Biology Program, Division of Biology, Kansas State University, Manhattan, KS 66506-4901, USA. detvisitsakun@hotmail.com <detvisitsakun@hotmail.com>

Virology
|April 27, 2007
PubMed

Insights

The Autographa californica M nucleopolyhedrovirus (AcMNPV) fibroblast growth factor (vfgf) gene impacts insect mortality. Deleting vfgf delays death when fed to insects, while overexpressing it accelerates death.

Area of Science:

  • Virology
  • Insect Pathology
  • Molecular Biology

Background:

  • The Autographa californica M nucleopolyhedrovirus (AcMNPV) fibroblast growth factor (vfgf) gene shares properties with cellular FGFs.
  • Previous studies showed vfgf deletion did not affect budded virus yield or viral synthesis in cell culture.

Purpose of the Study:

  • To characterize AcMNPV vfgf's role in insect hosts using different infection routes and developmental stages.
  • To investigate the impact of vfgf overexpression on AcMNPV infectivity and virulence.

Main Methods:

  • Characterization of AcMNPV deletion and overexpression mutants in Spodoptera frugiperda and Trichoplusia ni.
  • Infection routes included oral feeding and intrahemocoelic injection.
  • Assessment of viral infectivity, mortality, and budded virus production.

Main Results:

  • vfgf deletion did not affect AcMNPV infectivity but delayed host mortality upon oral feeding.
  • vfgf overexpression increased viral infectivity and accelerated host mortality in bioassays.
  • Overexpression of vfgf resulted in reduced budded virus production in cell culture.

Conclusions:

  • AcMNPV vfgf plays a role in efficient virus dissemination from the insect midgut.
  • The vfgf gene influences AcMNPV virulence and host mortality dynamics.

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