Prof. zur Hausen received his MD in 1960 from the University of Dusseldorf. After receiving further medical training, he was a research fellow first at the University of Dusseldorf 1962-1965, and then at the Children's Hospital of Philadelphia, 1966-1969, where he worked under Prof. Werner Henle. In 1969, he returned to Germany, at the University of Wurzburg, as a Senior Scientist at the Institute for Virology. During 1972-1977, he was the Chairman and Professor in the Institute for Clinical Virology at the University of Erlangen-Nurnberg, and then during 1977-1983 the Chairman and Professor at the Institute for Virology at the University of Freiburg. From 1983 until 2003, he was the Scientific Director and Chairman of the Management Board of the German Cancer Research Center (DKFZ) in Heidelberg. In 2003, he became an emeritus professor at the German Cancer Research Center. Prof. zur Hausen's laboratory has made several particularly noteworthy findings in papillomavirus research. The earliest was the recognition that there are multiple HPV genotypes, particularly that the HPVs that caused non-genital warts and those that caused genital warts might be distinct (2,3). Prior to his studies, it was believed that there might be a single HPV, as it had been shown in the first part of the 20th century that cutaneous warts could be induced with filtrates from genital or laryngeal warts.
His most important finding was the identification and molecular cloning of the HPV16 and HPV18 genomes, and the associated demonstration that a majority of cervical cancers contained DNA that hybridized under stringent conditions to probes from HPV16 or HPV18 and that an even higher proportion of cervical cancers would hybridize to these probes under less stringent conditions. These observations strongly implied: 1) papillomaviruses were etiologically involved in this cancer; 2) infection by more than one HPV type could result in cervical cancer; and 3) there were additional related HPV types that also caused cervical cancer. Indeed, subsequent research has indicated that infection by more than 10 other HPVs that are phylogenetically related to HPV16 and HPV18 are also in cervical cancer. HPV16 and 18 are the most oncogenic, accounting for about 70% of cervical cancer.The third critical finding was that the HPV DNA was integrated into the host genome in cervical cancer cell lines and the associated demonstration that the viral E6 and E7 genes were preferentially retained and expressed in the tumors. These observations provided a mechanism for the efficient transfer of viral DNA progeny cells, implied that viral gene expression might be required for maintenance of the tumorigenic phenotype, and that E6 and E7 probably represented key viral oncogenes.The findings related to HPV16 and HPV18 formed the basis for subsequent epidemiologic studies confirming that infection by a subset of HPV types, most notably HPV16 and HPV18, accounts for virtually all cervical cancers. In addition to the role of HPV in cervical cancer, other evidence has led to the conclusion that a substantial proportion of several additional types of cancer are also caused by HPV infection. These include various genital cancers (such as vulvar and penile cancers), anal cancers, and head-and-neck cancers.
Prof. zur Hausen has continued to run a highly productive laboratory since making the above seminal findings, publishing an average of more than 5 papers per year. Some of the more important findings made during this period include: 1) finding that most Buschke-Loewenstein tumors, which are large but low-grade malignant penile tumors, contain HPV6 or HPV11, which usually do not cause malignancy at other sites; determining that E6 and E7 expression in cervical cancer cell lines is required for maintaining the transformed phenotype; finding that HPV DNA in cervical tumors may be integrated near the c-Myc oncogene and be associated with its activation; the isolation of several new HPV types and their clinical importance; epidemiological studies delineating the prevalence of genital HPV infection and the risk of progression dysplasia or cancer; identification of cellular transcription factors that interact with the main HPV promoter; and the role of AP-1, Fos, and Fra-1 in regulating HPV transcription. He has also been a highly sought after and effective spokesman for the papillomavirus research community and for the role of viruses in human cancer.