Several DNA viruses have evolved antagonists to inhibit the cyclic GMP-AMP 
synthase (cGAS)-stimulator of interferon genes (STING) DNA-sensing immune 
pathway. This includes DNA viral oncogenes that antagonize the cGAS-STING 
pathway by binding STING through the LxCxE motif. The 293T human cells are 
widely used in biology studies as they are highly transfectable. While parental 
293 cells express high levels of STING, 293T cells lack STING and are unable to 
induce interferon antiviral responses to cytosolic DNA. Additionally, 293T cells 
express the SV40 polyomavirus large T antigen (LT) which enhances the 
replication of transfected DNA plasmids carrying the SV40 origin of replication. 
Since SV40 LT also encodes the LxCxE motif, the lack of STING expression in 293T 
cells is commonly assumed to be due to SV40 large T antigen. We find that SV40 
LT does not alter exogenously expressed and endogenous levels of STING protein. 
We show that STING transcription is suppressed in 293T cells but is not driven 
by SV40. This study also revealed that SV40 LT does indeed inhibit cGAS-STING 
interferon induction, but through a mechanism distinct from other DNA virus 
oncogenes. Collectively, these results indicate that while SV40 LT can inhibit 
cGAS-STING interferon induction, it does so in an unanticipated manner.