The most well studied cancer-related gene in history, p53, is responsible for protecting the integrity of the genome. A variety of different stresses are detected by p53 and its regulators, allowing for numerous post-translational modifications that activate p53. After activation p53 can then regulate transcription of a myriad downstream targets, resulting in either cell cycle arrest or apoptosis. One of the stress signals that activates p53 is viral infection in part through the induction of type-1 interferon. However some viruses, like the DNA tumor viruses have evolved factors capable of binding to p53 and inhibiting its ability to regulate its downstream factors in order to avoid cell cycle arrest or apoptosis and complete the viral life cycle. The human immunodeficiency virus (HIV), probably the most notorious virus of our time because of our inability to completely eradicate it from a host, is capable of activating p53 in certain cell types upon infection. Several studies have reported on the functions of p53 during HIV infection, such as inhibiting full-length transcription of HIV, interaction with a number of HIVencoded proteins such as the trans-activator of transcription (Tat), and eventual widespread apoptosis in T-cells, however these disparate roles are undoubtedly not the whole story. Our hypothesis is that an HIV factor, Tat is capable of mitigating the downstream effects of p53. To test this hypothesis we used U2-OS cells and created U2-OS cell lines that express Tat protein. These cells were then treated with the DNA damaging agents to activate p53. At various time post treatment, we measured promoter activity, mRNA and protein expression of p53 and its targets p21 and bax. Without further investigation, at the present time we have no convincing evidence that Tat inhibits p53 function
