TAT and infection: As the transcriptional function of Tat relies on nuclear localization, we hypothesized that if Tat could be sequestered in the cytoplasm by an Mpro-cleavable cytosolic membrane anchor such as the N-terminal myristoylation domain from the Src kinase, then Mpro-catalyzed cleavage during infection would cause relocalization of Tat to the nucleus to activate expression of a reporter construct.