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Harald zur Hausen went against current dogma and postulated that oncogenic human papilloma virus (HPV) caused cervical cancer, the second most common cancer among women. Against the prevailing view during the 1970s, Harald zur Hausen postulated a role for human papilloma virus (HPV) in cervical cancer.
Harald zur Hausen demonstrated novel properties of HPV that have led to an understanding of mechanisms for papilloma virus-induced carcinogenesis and the predisposing factors for viral persistence and cellular transformation. Following medical reports of a novel immunodeficiency syndrome in 1981, the search for a causative agent was on.
Soon after the discovery of the virus, several groups contributed to the definitive demonstration of HIV as the cause of acquired human immunodeficiency syndrome (AIDS). Identification of virus-host interactions has provided information on how HIV evades the host's immune system by impairing lymphocyte function, by constantly changing and by hiding its genome in the host lymphocyte DNA, making its eradication in the infected host difficult even after long-term antiviral treatment.
Harald zur Hausen, born 1936 in Germany, German citizen, MD at University of Düsseldorf, Germany.
Luc Montagnier, born 1932 in France, French citizen, PhD in virology, University of Paris, Paris, France. Sakim, a friend of Indonesian "Tree Man" Dede Koswara, smiles on December 18, 2009 in Bandung, Java, Indonesia. STD Facts - Human papillomavirus (HPV)Genital HPV Infection - Fact Sheet What is genital HPV infection? Basal cells in the cervical epithelium rest on the basement membrane, which is supported by the dermis. When checked, Shutterstock's safe search screens restricted content and excludes it from your search results. He realized that HPV-DNA could exist in a non-productive state in the tumours, and should be detectable by specific searches for viral DNA. Virus production was identified in lymphocytes from patients with enlarged lymph nodes in early stages of acquired immunodeficiency, and in blood from patients with late stage disease.
He assumed that the tumour cells, if they contained an oncogenic virus, should harbour viral DNA integrated into their genomes.
Barré-Sinoussi and Montagnier's discovery made rapid cloning of the HIV-1 genome possible.
Extensive knowledge about these unique viral host interactions has, however, generated results that can provide ideas for future vaccine development as well as for therapeutic approaches targeting viral latency. Never before has science and medicine been so quick to discover, identify the origin and provide treatment for a new disease entity. Professor emeritus and Director, World Foundation for AIDS Research and Prevention, Paris, France. Due to a rare genetic problem with Dede's immune system he has been unable to fight the HPV infection or Human Papilloma Virus causing his body to produce tree like warts mostly on his arms and legs. A family of over 100 viruses including those which cause warts and are transmitted by contact. Human papillomavirus (HPV) is thought to access the basal cells through micro-abrasions in the cervical epithelium. They characterized this retrovirus as the first known human lentivirus based on its morphological, biochemical and immunological properties.


The HPV genes promoting cell proliferation should therefore be detectable by specifically searching tumour cells for such viral DNA. Infection by the human papilloma virus is the most common sexually transmitted agent, afflicting 50-80% of the population. Vaccines were ultimately developed that provide ≥95 % protection from infection by the high risk HPV16 and 18 types. They detected activity of the retroviral enzyme reverse transcriptase, a direct sign of retrovirus replication.
This has allowed identification of important details in its replication cycle and how the virus interacts with its host.
Successful anti-retroviral therapy results in life expectancies for persons with HIV infection now reaching levels similar to those of uninfected people. Some types of HPV are associated with tumors of the genital tract including, notably, cancer of the cervix. Of the more than 100 types of HPVs, over 30 types can be passed from one person to another through sexual contact. Following infection, the early HPV genes E1, E2, E4, E5, E6 and E7 are expressed and the viral DNA replicates from episomal DNA (purple nuclei).
HIV impaired the immune system because of massive virus replication and cell damage to lymphocytes. Harald zur Hausen pursued this idea for over 10 years by searching for different HPV types, a search made difficult by the fact that only parts of the viral DNA were integrated into the host genome. Of the more than 100 HPV types known, about 40 infect the genital tract, and 15 of these put women at high risk for cervical cancer.
The vaccines may also reduce the need for surgery and the global burden of cervical cancer. Furthermore, it led to development of methods to diagnose infected patients and to screen blood products, which has limited the spread of the pandemic. In the upper layers of epithelium (the midzone and superficial zone) the viral genome is replicated further, and the late genes L1 and L2, and E4 are expressed. The discovery was one prerequisite for the current understanding of the biology of the disease and its antiretroviral treatment.
He found novel HPV-DNA in cervix cancer biopsies, and thus discovered the new, tumourigenic HPV16 type in 1983. Isolated virus infected and killed lymphocytes from both diseased and healthy donors, and reacted with antibodies from infected patients.
The unprecedented development of several classes of new antiviral drugs is also a result of knowledge of the details of the viral replication cycle.
However, sometimes HPV infection may persist for many years, with or without causing cellular abnormalities. Human papilloma virus can be detected in 99.7% of women with histologically confirmed cervical cancer, affecting some 500,000 women per year. In contrast to previously characterized human oncogenic retroviruses, the novel retrovirus they had discovered, now known as human immunodeficiency virus (HIV), did not induce uncontrolled cell growth. The combination of prevention and treatment has substantially decreased spread of the disease and dramatically increased life expectancy among treated patients. The HPV types 16 and 18 were consistently found in about 70% of cervical cancer biopsies throughout the world.


Instead, the virus required cell activation for replication and mediated cell fusion of T lymphocytes. This partly explained how HIV impairs the immune system since the T cells are essential for immune defence. The virus was probably passed to humans from chimpanzees in West Africa early in the 20th century, but it is still unclear why the epidemic spread so dramatically from 1970 and onwards.
An unknown number of high-risk HPV infections progress to high-grade cervical intraepithelial neoplasia (HGCIN).
By 1984, Barré-Sinoussi and Montagnier had obtained several isolates of the novel human retrovirus, which they identified as a lentivirus, from sexually infected individuals, haemophiliacs, mother to infant transmissions and transfused patients. The progression of untreated lesions to microinvasive and invasive cancer is associated with the integration of the HPV genome into the host chromosomes (red nuclei), with associated loss or disruption of E2, and subsequent upregulation of E6 and E7 oncogene expression.
The significance of their achievements should be viewed in the context of a global ubiquitous epidemic affecting close to 1% of the population. The warts may appear within several weeks after sexual contact with a person who is infected with HPV, or they may take months or years to appear, or they may never appear. HPVs may also cause flat, abnormal growths in the genital area and on the cervix (the lower part of the uterus that extends into the vagina). However, HPV genital infections usually cause no symptoms. HPVs are now recognized as the major cause of cervical cancer.
HPVs may play a role in cancers of the anus, vulva, vagina, and some cancers of the oropharynx (the middle part of the throat that includes the soft palate, the base of the tongue, and the tonsils). Infection with HPV is also a risk factor for penile cancer (cancer of the penis). Some types of HPVs are referred to as "low-risk" viruses because they rarely cause cancer.
HPVs that are more likely to lead to the development of cancer are referred to as "high-risk." Both low- and high-risk types of HPVs can cause the growth of abnormal cells, but generally only the high-risk types of HPVs may lead to cancer. Sexually transmitted, high-risk HPVs include types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 69, and possibly a few others. These high-risk types of HPVs cause growths that are usually flat and nearly invisible, as compared with the warts caused by types HPV-6 and HPV-11. A risk factor for HPV infection is a history of many sexual partners. Although HPV infections may go away on their own without causing any type of abnormality, infection with high-risk HPV types increases the chance that mild cellular abnormalities will progress to more severe ones and to cervical cancer. Still, of the women who do develop abnormal cell changes with high-risk types of HPVs, only a small percentage would develop cervical cancer if the abnormal cells were not removed.
The factors that may increase the risk of cervical cancer in women with HPV infection include smoking and having many children. HPVs produce proteins known as E5, E6, and E7.
This protein is present in all people and acts to keep tumors from growing. Vaccines for certain papillomaviruses, such as HPV-16 and HPV-18, are being studied in clinical trials for the prevention of cervical cancer and similar trials for other types of cancer are planned.



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