Co-infection of Manduca sexta larvae with polydnavirus from Cotesia congregata increases susceptibility to fatal infection by Autographa californica M Nucleopolyhedrovirus

Citation
Jo. Washburn et al., Co-infection of Manduca sexta larvae with polydnavirus from Cotesia congregata increases susceptibility to fatal infection by Autographa californica M Nucleopolyhedrovirus, J INSECT PH, 46(2), 2000, pp. 179-190
Citations number
31
Categorie Soggetti
Entomology/Pest Control",Physiology
Journal title
JOURNAL OF INSECT PHYSIOLOGY
ISSN journal
00221910 → ACNP
Volume
46
Issue
2
Year of publication
2000
Pages
179 - 190
Database
ISI
SICI code
0022-1910(200002)46:2<179:COMSLW>2.0.ZU;2-9
Abstract
We investigated pathogenesis of Autographa californica M Nucleopolyhedrovir us in the semipermissive host, Manduca sexta, using a lacZ recombinant viru s (AcMNPV-hsp70/lacZ) to track the temporal progression of infection. Resul ts from time course studies monitoring infections initiated orally in fourt h instars demonstrated that primary infection of midgut columnar cells bega n at 3 h post inoculation (hpi). We observed secondary infections in midgut -associated tracheae as early as 9 hpi, showing that the early events of pa thogenesis in M. sexta are similar to those of permissive noctuid larvae. I n M. sexta, however, unlike in permissive hosts, hemocytes rapidly surround ed infected tracheal cells and formed capsules. Subsequently, baculovims in fections failed to spread and ultimately were cleared, suggesting that a ce llular immune response had been triggered. To assess the effects of immunos uppression on baculovirus-induced disease, we compared the outcome of infec tions in immunocompetent hosts with those that were immunocompromised eithe r by parasitization with the braconid, Cotesia: congregata, or by injection of the parasitoid's polydnavirus. During the first 9 days after inoculatio n, parasitized and polydnavirus-inoculated M. sexta larvae died more quickl y and at higher levels than nonparasitized and sham-injected controls, sugg esting that the cellular immune response was a factor in conferring resista nce to fatal infection by AcMNPV-hsp70/lacZ (C) 2000 Elsevier Science Ltd. All rights reserved.