Abstract
The WHO estimates that nearly 10-15% of cancers have a known viral etiology, although this number is likely an underestimate. In glioblastoma (GBM), the most common primary brain malignancy, viral associations have been proposed and investigated without a definitive etiology. Viral-host interactions are known to alter cellular growth and stem cell programming, as well as modulate innate immune signaling. However, in GBM, the multifaceted role of endogenous or exogenous viral expression remains unclear. Here, we provide a review of common viral associations in GBM and discuss how these viruses modulate intrinsic cellular processes to enhance anti-viral immune response or suppress anti-tumor immunity.