INBRE

Direct viral infection and subsequent replication in susceptible primary host cells is critical in identifying cell and tissue tropism, mechanisms of viral replication, and host cell disease physiology. Recently the Moore and Chow laboratories have developed a protocol for the large scale production of primary cell cultures using embryonic cells from the nematode, C. elegans. These primary cells are then used as targets for infection with Vesicular Stomatitis Virus (VSV). This preliminary work has concluded that VSV does infect C. elegans primary cells as seen by fluorescence of target cells after infection with VSV-GFP. In addition, RT-PCR analysis of infected primary cells indicates expression of viral N protein mRNA. With the use of tissue-specific GFP transgenics worms, it has been shown that VSV specifically targets neuronal cells of the worm. Primary cells from C. elegans can therefore be used as a simple model for viral infections. One of the long-term goals of this work is to determine the role of innate immunity in the regulation of viral replication and infection. RNAi appears to play an important role in the regulation of VSV infection of primary C. elegans cells as determined by increased infection rates of RNAi mutant cells compared to cells from the N2 wildtype. Apoptosis has been also hypothesized to be another defense mechanism. This is the current focus of our studies. To support the disease model and further determine the role of apoptosis in the regulation of viral infection, the Specific Aim of this proposal is two-fold: 1) to determine the consequence of VSV infection on primary cells from C. elegans, and 2) to determine the consequence of cellular responses (i.e., apoptosis) on viral infection.

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Updated 10/31/2005

The Arkansas INBRE is Supported by a grant from the National Institutes of Health
and the National Center for Research Resources (P20 RR-16460).

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