Central role of hemocytes in Autographa californica M nucleopolyhedroviruspathogenesis in Heliothis virescens and Helicoverpa zea

Autographa californica M nucleopolyhedrovirus (AcMNPV) can infect and kill a wide range of larval lepidopteran hosts, but the dosage required to achie ve mortal infection varies greatly. Using a reporter gene construct, me ide ntified key differences between AcMNPV pathogenesis in Heliothis virescens and Helicoverpa zea, a fully permissive and a semipermissive host, respecti vely. Even though there was more than a 1,000-fold difference in the suscep tibilities of these two species to mortal infection, there was no significa nt difference in their susceptibilities to primary infections in the midgut or secondary infections in the tracheal epidermis. Foci of infection withi n the tracheal epidermis of H. zea, however, were melanized and encapsulate d by 48 h after oral inoculation, a host response not observed in H. viresc ens, Further, H. zea hemocytes, unlike those of H. virescens, were highly r esistant to AcMNPV infection; reporter gene expression was observed only ra rely even though virus mas taken up readily, and nucleocapsids were transpo rted to the nucleus. Collectively, these results demonstrated that hemocyte s--by removing virus from the hemolymph instead of amplifying it and bg par ticipating in the encapsulation of infection foci--together with the host's melanization response, formed the basis of H. zea's resistance to fatal in fection by AcMNPV.