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Journal of Virology, January 2001, p. 996-1003, Vol. 75, No. 2
Department of Plant and Microbial Biology,
University of California, Berkeley, California 94720-3102
Received 7 August 2000/Accepted 16 October 2000
Autographa californica M nucleopolyhedrovirus
(AcMNPV) can infect and kill a wide range of larval
lepidopteran hosts, but the dosage required to achieve mortal infection
varies greatly. Using a reporter gene construct, we identified key
differences between AcMNPV pathogenesis in Heliothis
virescens and Helicoverpa zea, a fully permissive and
a semipermissive host, respectively. Even though there was more than a
1,000-fold difference in the susceptibilities of these two species to
mortal infection, there was no significant difference in their
susceptibilities to primary infections in the midgut or secondary
infections in the tracheal epidermis. Foci of infection within the
tracheal epidermis of H. zea, however, were melanized and
encapsulated by 48 h after oral inoculation, a host response not
observed in H. virescens. Further, H. zea
hemocytes, unlike those of H. virescens, were highly
resistant to AcMNPV infection; reporter gene expression was
observed only rarely even though virus was taken up readily, and
nucleocapsids were transported to the nucleus. Collectively, these
results demonstrated that hemocytes
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.2.996-1003.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Central Role of Hemocytes in Autographa
californica M Nucleopolyhedrovirus Pathogenesis in Heliothis
virescens and Helicoverpa zea
by removing virus from the
hemolymph instead of amplifying it and by participating in the
encapsulation of infection foci
together with the host's melanization response, formed the basis of H. zea's resistance to fatal
infection by AcMNPV.
*
Corresponding author. Mailing address: 251 Koshland
Hall, University of California, Berkeley, CA 94720-3102. Phone: (510) 642-4500. Fax: (510) 642-4995. E-mail:
lvolkman{at}nature.berkeley.edu.
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