@entity4538 gene expression in long-term infected XXXX stem cells.

@entity1 @entity38054 @entity650 @entity1313 @entity5 @entity4104 @entity4731 @entity11 @entity4538 @entity463
The most common adult primary @entity1313 , @entity463 ( @entity463 ), is characterized by fifteen months median @entity1 survival and has no clear etiology. We and others have identified the presence of @entity4538 ) gene products endogenously expressed in @entity463 tissue and primary cells, with a subset of viral genes being consistently expressed in most samples. Among these viral genes, several have important oncomodulatory properties, regulating @entity5 stemness, proliferation, immune evasion, invasion and angiogenesis. These findings lead us to hypothesize that a specific HCMV gene signature may be associated with @entity463 pathogenesis. To investigate this hypothesis, we used @entity11 cell lines and @entity11 stem-like cells (GSC) infected with clinical and laboratory HCMV strains and measured relative viral gene expression levels along several time points up to 15 weeks post-infection. While HCMV gene expression was detected in several infected @entity11 lines through week 5 post-infection, only HCMV-infected GSC expressed viral gene products 15 weeks post-infection. Efficiency of infection across time was higher in GSC compared to cell lines. Importantly, HCMV-infected GSC outlived their uninfected counterparts, and this extended survival was paralleled by increased tumorsphere frequency and upregulation of stemness regulators, such as @entity4731 , p- @entity4104 , and @entity38054 (a novel HCMV target identified in this study). @entity650 ( @entity650 ) treatment significantly upregulated HCMV gene expression in long-term infected @entity11 , suggesting that pro-inflammatory signaling in the @entity5 milieu may further augment HCMV gene expression and subsequent @entity5 progression driven by viral-induced cellular signaling. Together, our data support a critical role for long-term, low-level HCMV infection in promoting survival, stemness, and proliferation of GSC that could significantly contribute to @entity463 pathogenesis.
