As previously mentioned, the squamous epithelium acts as a protective ‘skin’ to keep pathogens from infecting the underlying tissue. Even though the cervix is not an externally exposed tissue it is still subject to the external environment, especially during sexual intercourse. The HPV is able to get through the protective layers of the squamous epithelium through epithelial abrasions to commence its infective life cycle.
Figure 3.7 Schematic diagram of infection of squamous epithelium by HPV (Figure 2 from Frazer 2004)
Incidence in Europe as a whole was seventh in frequency and mortality fifth.
Incidence and mortality between countries in Europe varies according to the risk of disease and effectiveness of population screening.
HPV 16 is the most frequent high-risk type in cervical cancer Europe; HPV 16, 18 and 45 are the most frequent types in adenocarcinoma.
Apart from factors related to exposure to high-risk HPV, cigarette smoking, immunosuppression and poor diet are among risk factors for cervical cancer and its precursors.
HPV gains access to the basal layer of the cervical epithelium in order to infect the cervix.
Productive infection with high-risk and low-risk types of HPV is usually self-limiting; persistent HPV carries a risk of progression.
Development of high-grade precancerous lesions and cancer in a minority of women depends on integration of viral DNA into the host genome and consequent blocking of regulatory enzymes.
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