

Jennifer Berrier Kincaid (Creator)
The University of North Carolina at Greensboro (UNCG )
Web Site: http://library.uncg.edu/
Amy Adamson

Abstract: The Influenza A virus leads to yearly epidemics and occasional world-wide pandemics, as with the Spanish Influenza of 1918. The frequent mutation rate of the virus mandates that new vaccines be created often. Additionally, acquired resistance to antiviral drugs makes them less effective over time. Cellular targets, that have a much lower rate of mutation, provide possible targets for new therapies that can withstand viral genetic drift. The goal of this study was to identify possible cellular targets which modulate the function of the M2 viral protein, and therefore affect the replication cycle. To obtain this goal, the second-site modifier screen in Drosophila melanogaster was employed to test approximately 1,200 gene disruptions for their effects on M2 activity. To first establish the model system as a reliable testing tool, flies expressing M2 were exposed to amantadine, a known M2 blocker. It was shown that M2 functions as an ion channel in the fly, as in human hosts; and, that amantadine blocks this activity, thus supporting our use of the model system. Subsequently, the mutant stocks were screened for changes in rough eye phenotype of M2 expressing flies, followed by control verifications. Of the stocks screened 9 candidates were selected for future studies. These genes represent possible cellular targets for future antiviral therapies.

Additional Information

Language: English
Date: 2010
amantadine, antiviral, Influenza A, M2, Viral proteins
Influenza A Virus $x Research.
Viruses $x Reproduction.
Amantadine $x Research.
Virus inhibitors.
Drosophila melanogaster.

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