Faculty and Research
Faculty by Name
Loy Volkman
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Loy Volkman
Research Interests
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Our group studies pathogenesis induced by a virus that infects the larvae of lepidopteran insects (moths/butterflies) called Autographa californica M nucleopolyhedrovirus (AcMNPV). The study of this virus provides an opportunity to contribute to the development of biological alternatives to chemical pesticides, as well as to gain insight into the molecular and cell biology of the target organisms and virus-cell interactions.
AcMNPV is the best-studied member of Baculoviridae, a family of viruses restricted to arthropod hosts. Perhaps because of the strict co-evolution of these viruses with their invertebrate hosts, certain aspects of their replicative strategy are not shared by viruses of vertebrates or plants. One unique property recently established, for example, is that actin is essential for the assembly of AcMNPV nucleocapsids. While actin has long been known to be involved in the budding of many enveloped viruses, such a dependence on actin for the assembly of a virus in the nucleus has never been reported before.
Current Projects
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One focus of current research is the elucidation of the viral gene products involved in the manipulation of the actin cytoskeleton. The availability of the complete AcMNPV genome sequence and evidence that two viral structural proteins (components of the capsid) are actin-binding proteins provide convenient vantage points from which to investigate this problem. In addition to assembly, evidence suggests that actin is also involved in the transport of AcMNPV nucleocapsids to the nucleus. This problem is also under investigation.
Another focus of research is the comparison of viral pathogenesis in larval insect hosts of varying susceptibilities. Our approach is to use recombinant viruses equipped with reporter genes to compare the progress of infection in susceptible and resistant hosts. This approach has yielded valuable information about important benchmarks of the infection process, as well as identifying resistance barriers in less susceptible hosts. For example, we have learned that decreasing susceptibility of aging insects is a midgut-related phenomenon; that the midgut is cleared of infection during molting; that the insect's tracheal (respiratory) system, the second tissue infected, is the conduit used by the virus for spreading infection within the host and that within highly susceptible hosts, infection of the tracheal system portends death. Infection of tracheal cells leads to infection of hemocytes, and recently we determined that the inability of hemocytes of the corn ear worm, Helicoverpa zea, to support AcMNPV replication accounts for the majority of theextreme resistance to mortal infection observed in that host. In the fall armyworm, Spodoptera frugiperda, it is the midgut cells that confer organismal protection to infection, as other cell types are highly susceptible. We are using various genetic and cell biological approaches to elucidate the underlying cause of the observed tissue-specific resistances in both hosts.
Finally, the hallmark of baculovirus-induced pathology is liquefaction of the host. This dramatic ending is coincident with death and is mediated by two virus-encoded enzymes, a cathepsin and a chitinase. We are interested in illuminating the interaction and regulation of these two enzymes.
Selected Publications
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WASP homology sequences in baculoviruses: remarkable evolutionary conservation and striking contrasts. [L.M. Machesky, R.H. Insall, and L.E.Volkman. (2001) Trends Cell Biol., 11, 286-287]
The central role of hemocytes in Autographa californica M nucleopolyhedrovirus pathogenesis in Heliothis virescens and Helicoverpa zea. [D. Trudeau, J. O. Washburn and L.E.Volkman (2001) J. Virol. 75, 996-1003]
Autographa californica M nucleopolyhedrovirus chiA is required for processing of V-CATH. [L. G. Hom and L.E. Volkman (2000) Virology 277, 178-183]
Filamentous actin is required for lepidopteran nucleopolyhedrovirus progeny production. [L.Kasman and L.E. Volkman (2000) J. Gen. Virol. 81, 1881-1888]
Direct proof that nuclear F-actin is essential for AcMNPV morphogenesis. [T. Ohkawa and L.E. Volkman (1999) Virology 264, 1-4]
Multiple nucleocapsid packaging of Autographa californica M nucleopolyhedrovirus accelerates the onset of systemic infection in Trichoplusia ni. [J.O. Washburn, E. Lyons, E. Haas-Stapleton and L.E. Volkman (1999) J. Virol. 73, 411-416]
Acting binding and nucleation by Autographa californica M nucleopolyhedrovirus. [L.M.Lanier and L.E. Volkman (1998) Virology 243, 167-177]
Nucleopolyhedrovirus interactions with their insect hosts.[L.E. Volkman (1997) Adv. Virus Res. 48, 313-348]
Insect protection against viruses. [J. O.Washburn, B. A. Kirkpatrick and L. E.Volkman (1996) Nature 383, 767]
The insect tracheal system: A conduit for the systemic spread of Autographa californica nuclear polyhedrosis virus. [K. K. Engelhard, L. N. W. Kam-Morgan, J. O. Washburn and L. E. Volkman (1994) Proc.Natl. Acad.Sci.USA 91, 3224-3227]
Sequential rearrangement and nuclear polymerization of f-actin in baculovirus-infected insect cells. [C. A. Charlton and L. E. Volkman (1991) J. Virol. 65, 1291-1227]
Last Updated 2004-07-30