The epidemiology of human papillomavirus infections.

Background It is uncertain whether male circumcision reduces the risks of penile human papillomavirus (HPV) infection in the man and of cervical cancer in his female partner. Methods We pooled data on 1913 couples enrolled in one of seven case–control studies of cervical carcinoma in situ and cervical cancer in five countries. Circumcision status was self-reported, and the accuracy of the data was confirmed by physical examination at three study sites. The presence or absence of penile HPV DNA was assessed by a polymerase-chain-reaction assay in 1520 men and yielded a valid result in the case of 1139 men (74.9 percent). Results Penile HPV was detected in 166 of the 847 uncircumcised men (19.6 percent) and in 16 of the 292 circumcised men (5.5 percent). After adjustment for age at first intercourse, lifetime number of sexual partners, and other potential confounders, circumcised men were less likely than uncircumcised men to have HPV infection (odds ratio, 0.37; 95 percent confidence interval, 0.16 to 0.85...

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Male circumcision, penile human papillomavirus infection, and cervical cancer in female partners

ISSUES Cervical squamous cell carcinomas, adenocarcinomas and their precursors are caused by the human papillomavirus (HPV). Although HPV appears to be essential to the transformation of these epithelial cells, it is not sufficient, and a variety of cofactors and molecular events must take place between when an HPV infection occurs and a cervical cancer or its precursor develops. This review examines the data supporting these contentions, briefly outlines the molecular events that occur, considers the epidemiology and natural history of the disease, and details the implications of using HPV detection and typing in both clinical management and population-based screening programs. CONSENSUS POSITION 1. Based on the available molecular, clinical and epidemiologic data, a subset of HPVs are unequivocally the etiologic agents for cervical cancers and their precursors. 2. Different mucosotropic HPVs have varying neoplastic potential. However, the great majority of cervical HPVs have oncogenic potential. Since oncogenic HPV-induced epithelial transformation to a high grade lesion or cancer is rare relative to the rate of infection, the term high risk is discouraged. 3. HPV's interaction with host cells has two principal biologic consequences: a) All anogenital HPVs induce low grade squamous lesions, which are the morphologic correlate of a productive infection. b) Rarely, HPVs induce a proliferative epithelial phenotype that pathologists recognize as a high grade lesion and that is the proximate cytohistologic precursor of invasive cervical carcinoma. 4. HPV biology and issues of practical clinical management should be reflected in the classification systems used for cytologic and histologic diagnosis. ONGOING ISSUES The molecular identification of HPVs (HPV testing) potentially may be very useful for primary screening or secondary triage of patients with certain lesions. However, the technology available to the practicing clinician is still evolving. Optimization of type spectrum, sensitivity, specificity and ease of use is under development. Data regarding these factors as well as a clear cost benefit analysis are sparse or pending in several large trials. Until such data are available, caution in clinical implementation of HPV testing is warranted.

Human papillomavirus. International Academy of Cytology Task Force summary. Diagnostic Cytology Towards the 21st Century: An International Expert Conference and Tutorial.

The view that common warts (verrucae vulgares), juvenile warts (verrucae planae), and genital warts (condylomata acuminata) are caused by the same virus and that differences in appearance are the result of variations in location and host reactivity has been shared by dermatologists for several decades (Frey, 1924; Waelsch and Habermann, 1924; Young, 1964; Rowson and Mahy, 1967; Nasemann, 1974; Lever and Schaumburg-Lever, 1975). This has probably reduced the interest in specific types of human papillomas.

Human papillomaviruses and their possible role in squamous cell carcinomas.

http://www.hu.ufsc.br/projeto_hpv/Immune%20responses%20to%20human%20papillomavirus.pdf

Immune responses to human papillomavirus.

Genital warts were known to the ancients, and many Greek and Roman writers referred to them. The early history of the disease has recently been reviewed by Bafverstedt (1967), who pointed out that some of the early synonyms for the lesions, particularly the words 'fig' and 'condyloma', have survived into modern times. In the Middle Ages, descriptions of diseases were less precise than in the ancient world, but some of the genital lesions described (Lanfranc, 1306) may have been warts. The outbreak of syphilis in Europe at the end of the 15th century led to renewed interest in genital diseases, but at this time most genital lesions were attributed to the 'venereal poison', and no causal distinction was made between the diseases now known as gonorrhoea, syphilis, and genital warts. Even Hunter (1786), who gave a clear description of genital warts, regarded them as a manifestation of syphilis, and did not differentiate them from condylomata lata. The important recognition that genital warts comprised a disease entity unrelated to syphilis was first made by Bell (1793), and his work was later confirmed by Jourdan (1826) and Ricord (1838). But, as the belief that genital warts were due to syphilis was gradually abandoned, the erroneous view developed that they were connected with gonorrhoea (Pirrie, 1852); indeed, in the 19th century, they were sometimes referred to as 'gonorrhoeal warts'. But Aime Martin (1872) pointed out that many patients with genital warts gave no history of gonorrhoea, and after the isolation of the gonococcus in 1879 it was realised that over half of the patients with genital warts showed no sign of it (Jadassohn, 1905). Many 19th century writers thought that genital warts were caused by irritation of the epidermis by various agents such as dirt, decomposed smegma, and genital discharges (Astley Cooper, 1835; Bumstead, 1864). This 'non-specific irritant' theory was widely accepted for many years; Cronquist (1912) strongly supported it, and it was reaffirmed well into the 20th century (Kaplan, 1942).

https://sti.bmj.com/content/sextrans/47/1/1.full.pdf

J D Oriel

Papers

Natural history of genital warts.