Early pathogenesis of Autographa californica multiple nucleopolyhedrovirus and Helicoverpa zea single nucleopolyhedrovirus in Heliothis virescens: a comparison of the 'M' and 'S' strategies for establishing fatal infection.

Nucleopolyhedroviruses (NPVs) (Baculoviridae) produce fatal infections in larval lepidopteran insects. NPVs are designated SNPVs or MNPVs based on whether the occlusion-derived virus (ODV) that initiates primary midgut infections contains single (S) or multiple (M) nucleocapsids. The principal consequence of this ODV packaging is that primary target cells infected with the M phenotype receive multiple nucleocapsids, whereas those infected by the S phenotype receive only one. To determine the biological significance of this difference in the initial infection strategy, a comparison of the primary and secondary infection patterns of the recombinants Helicoverpa zea SNPV (HzSNPV-hsp70/lacZ) and Autographa californica MNPV (AcMNPV-hsp70/lacZ) in orally inoculated larvae of Heliothis virescens was carried out. At dosages yielding similar final mortalities ( approximately 85 %), primary midgut infections by HzSNPV-hsp70/lacZ (indicated by lacZ expression) were observed 6 h earlier and in greater numbers than those generated by AcMNPV-hsp70/lacZ. Infection of secondary target cells in the tracheal epidermis, however, occurred at the same time and at the same rate for both NPVs. A 2 h delay was observed between the onset of primary and secondary AcMNPV-hsp70/lacZ infection, supporting the hypothesis that early tracheal infections were initiated by ODV nucleocapsids repackaged as budded virus. In contrast, an 8 h delay was observed with HzSNPV-hsp70/lacZ, suggesting that systemic infections were established only after virus replication in primary targets. Significant numbers of both MNPV- and SNPV-infected primary target cells were sloughed from the midgut beginning as early as 16 h post-infection. Midgut cell sloughing may be an important host-mediated selection pressure influencing the evolution of NPV morphology and gene regulation, shaping, in part, baculovirus infection strategies.