Human papillomaviruses (HPV) infect epithelial cells and bring about the formation of hyperproliferative lesions. Around 100 different types of HPV have been identified, many of which infect the genital tract and produce genital warts. Some HPV types are associated with cancer. HPV DNA can be detected in virtually all cervical cancers (99.7%) and these viruses are acknowledged to be a causative agent of this disease. In addition, HPVs might be involved in other malignant diseases including cancer of the vulva, oral cancer, and skin cancer. The papillomavirus E2 protein regulates transcription of the HPV genome and is also required for viral replication. Recent work suggests that the E2 protein is a suitable target for drug research and might itself be a useful clinical tool. Drugs that inhibit E2 function would be expected to prevent HPV replication and to be of value in the treatment of HPV infections. Since HPV replication is thought to precede HPV-induced tumourigenesis, these drugs might also prevent cancer. Over-expression of the E2 protein can block the proliferation of cervical cancer cells. If E2 can be delivered to cancer cells in vivo, this protein might be an effective cancer treatment.

Around 100 types of human papillomavirus (HPV) have been identified, many of which infect the genital tract. The so-called, low-risk HPV types (LR-HPV), such as HPV 6 and HPV 11, bring about the formation of benign genital warts [1]. In contrast, the high-risk HPV types (HR-HPV), such as HPV 16 and HPV 18, are a causative agent of cervical cancer, a disease responsible for over 10,000 deaths per year in the European Union alone [2]. This review will focus on the papillomavirus E2 protein and recent work that seeks to use this protein as either a clinical target, or a clinical tool, in the treatment of HPV infection and HPV-induced tumourigenesis.