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Dysregulated viral gene expression is directly correlated with altered EBV chromatin looping We determined that the type III latency EBV genome establishes a complex network of intragenomic interactions and that PARP1 inhibition alters viral gene expression as well as the occupancy of both CTCF and cohesin chromatin looping factors

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This view suggests that semaglutide captures most of the available benefit from incretin-based therapy, and tirzepatide’s advantage comes from fine-tuning rather than fundamentally different mechanisms