FRI-758 Does Sattabacin Inhibit Viral Replication of the Varicella Zoster Virus in Human Epithelial Cells?

Friday, October 12, 2012: 7:20 PM
Hall 4E/F (WSCC)
Serena Mancha , Fort Lewis College, Durango, CO
Kenneth Miller , Fort Lewis College, Durango, CO
David Blake , Fort Lewis College, Durango, CO
Introduction: Herpes simplex virus 3 (HSV3) is commonly known as the Varicella zoster virus (VZV), which is a DNA virus within the Herpesviridae family.  Infection with VZV in children results in chickenpox (varicella), and reactivation of the virus in the elderly or in immunocompromised adults leads to shingles (zoster).

Hypothesis: We hypothesize that sattabacin and other structurally related compounds will have anti-viral activity against VZV infection in human fibroblast cells (MRC-5 cell line).

Methods: Our study utilizes sattabacin, 4-hydroxysattabacin and sattazolin, which have been synthetically produced in the Chemistry Department, and are known to exhibit antiviral activity. To identify effective anti-viral compounds against VZV infection a traditional viral plaque assay will be performed. Microarray analysis will also be used to determine a cellular mechanism by which these compounds inhibit VZV replication by analyzing global gene expression changes in human fibroblast cells.

Results: Human fibroblast cells were exposed to various concentrations of each compound for up to 6 hours and cell viability was assessed. Sattabacin and its derivatives were cytotoxic at concentrations greater than 100 mM. Our preliminary results indicate that VZV infects human fibroblasts and leads to cytopathic effects, which were quantified through the NIH Image J software. Finally, we propose to identify a possible cellular mechanism by which the most potent anti-viral compound inhibits VZV replication through microarray analysis. Our results will provide important information regarding VZV infection in humans as well as identify essential anti-viral cellular mechanisms.