Varicella zoster virus (VZV) is a human alphaherpesvirus that causes varicella (chickenpox) during primary infection. During varicella, VZV establishes life long latency in the dorsal root ganglia and can later reactivate to cause herpes zoster (shingles). This reactivation can cause serious complications, one of the most prevalent being post-herpetic neuralgia (PHN)- a severe neuropathic pain, which lasts at least 3 months beyond the appearance of the herpes zoster rash. The mechanisms by which VZV establishes latency and can later reactivate to cause herpes zoster and PHN are not fully understood; however it has been suggested that viral inhibition of neuronal apoptosis may play an important role. We have previously shown that VZV ORF63 can inhibit neuronal apoptosis, however the mechanism of action is yet to be elucidated. To study the effects of VZV ORF63 on the apoptosis pathway, human foreskin fibroblasts (HFFs) were transduced with a novel lentivirus encoding VZV ORF63 with expression and functionality of ORF63 confirmed via western blotting, flow cytometry and immunofluorescence assay (IFA) analysis. Apoptosis was induced in transduced cells through treatment with a protein kinase inhibitor, staurosporine, and the percentage of apoptotic cells was determined via the detection of cleaved caspase 3 (CC3) by IFA. Comparison of ORF63 expressing HFFs to parental transduced HFFs, revealed a statistically significant 22% reduction in CC3 positive cells with ORF63 expression. This finding was supported by western blot analysis for caspase 3 and CC3, which confirmed significantly less CC3 was present in staurosporine treated ORF63 transduced cells. Together these data indicate that VZV ORF63 protects HFFs from staurosporine-induced apoptosis. Furthermore this work validates a model that could be applied to determine the mode of action of VZV ORF63 in the protection of neurons from apoptosis, thereby increasing our understanding of how VZV latency is established and maintained.