Comparative pathogenesis of Helicoverpa zea S nucleopolyhedrovirus in noctuid larvae

Citation
Jo. Washburn et al., Comparative pathogenesis of Helicoverpa zea S nucleopolyhedrovirus in noctuid larvae, J GEN VIROL, 82, 2001, pp. 1777-1784
Citations number
25
Categorie Soggetti
Microbiology
Journal title
JOURNAL OF GENERAL VIROLOGY
ISSN journal
00221317 → ACNP
Volume
82
Year of publication
2001
Part
7
Pages
1777 - 1784
Database
ISI
SICI code
0022-1317(200107)82:<1777:CPOHZS>2.0.ZU;2-1
Abstract
We used a recombinant of Helicoverpa tea S nucleopolyhedrovirus containing the hsp70/lacZ reporter cassette (HzSNPV-hsp70/lacZ) to quantify mortality relationships and to elucidate early pathogenesis in two permissive hosts, Heliothis virescens and Helicoverpa tea, and one semipermissive host, Trich oplusia ni, Fourth instar T. ni were highly resistant to fatal infection bo th by oral injection of occlusions and by intrahaemocoelic injection of bud ded virus, indicating the presence of both midgut and systemic mechanisms o f resistance. In bioassays, newly moulted (4(0)) H. tea were significantly more susceptible than 4(0) H, virescens to fatal infection, but mortality l evels were the same for larval cohorts inoculated 16 h after the moult (4(1 6)), Developmental resistance was stronger in H, tea and in both hosts, par tially reversed by administration of the optical brightener M2R, In both sp ecies, developmental resistance was correlated with a reduced ability of Hz SNPV to establish and/or maintain primary midgut infections, in time-course experiments using a dosage of 15 occlusions (similar to LD90), lacZ expres sion marking the onset of primary and secondary infection was first observe d in midgut columnar and tracheal cells at 4 and 12 h, respectively, Inocul ation of 4(0) larvae resulted in approximately twofold more foci in H, tea larvae than in H. virescens, but H, tea larvae sloughed infected midgut cel ls at a faster rate. For both heliothines, interaction of occlusion-derived virus with primary cellular targets within the midgut epithelium was criti cal to the outcome of infection and a key process underlying acquisition of developmental resistance.