The human papilloma virus, or HPV, is the second most common sexually transmitted pathogen in the world, as well as the main cause of cervical cancer, though it has also started to be increasingly associated with colon and throat cancer over the years. There are many HPV types, of which, HPV16 causes infections that show the highest risk of turning into cancer. HPV16, like other HPV types that may progress into cancer, depends on a tightly regulated expression of the early genes to regulate infection. Proteins expressed by early genes like E1 and E2 regulate the expression of other early genes and make the DNA polymerase more readily available for viral replication, while E6 and E7 more directly associate with the development of cancer, maintaining a constant state of division and blocking apoptosis. As such, the E6E7 CDS is of particular interest to understanding the processes behind tumorigenesis from HPV infections. In high-risk HPV types, like HPV16, the expression of these genes is regulated by post-transcriptional changes, in processes like alternative splicing, the process by which different sections of a pre-mRNA may be spliced out to express different products. Vaccination for HPV16, and other types, is available and very effective, but post-exposure therapy for this virus has not been developed. However, by understanding the specific mechanisms behind HPV early gene regulation, it may be possible to identify therapy targets. The HPV genome has different genetic elements that interact to regulate expression, like splice sites or splicing enhancers and silencers. As such, in this project, we attempted to construct, characterize and study reporter plasmids containing different sections of the E6E7-coding region, to better understand how this region individually regulates the expression of HPV16’s early genes, in hopes of developing a strong tool to study this virus.