D0415 Systemic pathogenesis of AcMNPV in Anticarsia gemmatalis larvae

Wednesday, December 16, 2009
Hall D, First Floor (Convention Center)
Eric Haas-Stapleton , Biological Sciences, California State University-Long Beach, Long Beach, CA
Tiffany Chen , Biological Sciences, California State University-Long Beach, Long Beach, CA
Alisa De La Cruz , Biological Sciences, California State University-Long Beach, Long Beach, CA
Elisa Martinez , Biological Sciences, California State University-Long Beach, Long Beach, CA
Marianne Torres , Biological Sciences, California State University-Long Beach, Long Beach, CA
We have investigated infection and pathogenesis of Autographa californica multiple nucleopolyhedrovirus in penultimate instar Anticarsia gemmatalis (velvetbean caterpillar), using a lacZ recombinant virus (AcMNPV-hsp70/lacZ) to track the temporal progression of infection in the hemocoel. A. gemmatalis was resistant to fatal infection by budded virus (BV) administered via the systemic route (LD50>3 x 105 BV). Time-course studies showed BV did not efficiently disseminate infection and only cuticular epidermal cells displayed relatively high levels of viral infection. Flow cytometry analysis of hemocytes isolated from BV‐inoculated A. gemmatalis larvae showed low level expression of the BV envelope protein GP64 on the cell surface, pointing to a limited capacity for A. gemmatalis hemocytes to amplify virus in the insect. However, hemocytes infected ex vivo with AcMNPV-hsp70/lacZ produced LACZ, suggesting that BV can enter and uncoat in hemocytes. Cell-free hemolymph isolated from A. gemmatalis reduced BV infectivity relative to hemolymph isolated from Trichoplusia ni, a species permissive to AcMNPV. In aggregate, our studies suggest that systemic AcMNPV infection of A. gemmatalis is limited by inefficient BV amplification and components of hemolymph specific to A. gemmatalis that reduce BV infectivity.

doi: 10.1603/ICE.2016.44431