1887

Abstract

We used a recombinant of S nucleopolyhedrovirus containing the / reporter cassette (HzSNPV-/) to quantify mortality relationships and to elucidate early pathogenesis in two permissive hosts, and , and one semi-permissive host, . Fourth instar were highly resistant to fatal infection both by oral injection of occlusions and by intrahaemocoelic injection of budded virus, indicating the presence of both midgut and systemic mechanisms of resistance. In bioassays, newly moulted (4) were significantly more susceptible than 4 to fatal infection, but mortality levels were the same for larval cohorts inoculated 16 h after the moult (4). Developmental resistance was stronger in and in both hosts, partially reversed by administration of the optical brightener M2R. In both species, developmental resistance was correlated with a reduced ability of HzSNPV to establish and/or maintain primary midgut infections. In time-course experiments using a dosage of 15 occlusions (∼LD), expression marking the onset of primary and secondary infection was first observed in midgut columnar and tracheal cells at 4 and 12 h, respectively. Inoculation of 4 larvae resulted in approximately twofold more foci in larvae than in , but larvae sloughed infected midgut cells at a faster rate. For both heliothines, interaction of occlusion-derived virus with primary cellular targets within the midgut epithelium was critical to the outcome of infection and a key process underlying acquisition of developmental resistance.

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2001-07-01
2019-12-11
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