Abstract

Endometriosis is a chronic disease in which endometrium-like lesions are located ectopically, frequently in the pelvic cavity but also in more distant regions. It has been estimated that 5 to 10% of fertile women are suffering from the disease, and in a population of women with dysmenorrhoea (painful periods), around 50% have endometriosis (Faquhar, 2007). The symptoms include chronic pelvic pain, dysmenorrhoea, dyspareunia (pain during intercourse), and subfertility. The pathogenesis of endometriosis is unclear. Endometriosis is hormonal-dependent and therefore mainly found in women in the fertile age, although rare cases have been found in men and postmenopausal women. The risk is increased sevento nine-fold for women who have a close relative (mother and/or sister) with endometriosis, indicating some genetic involvement (Simpson et al., 1980). Endometriosis displays malignant-like features, such as invasiveness and metastasis, and DNA viruses might play a role in endometriosis, like human papillomavirus (HPV) is part of the pathogenesis of cervix cancer (zur Hausen, 2009). Signs of inflammation are the key findings in endometriosis. From the above, some evidence points towards a possible involvement of the type I interferons (IFNs). This chapter will discuss whether DNA-viruses and the innate immune system might be involved in the pathogenesis of endometriosis.

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