Cervical cancer is a malignant epithelial tumor that affects the vaginal part of the cervix or cervical canal, and nowadays about 500.000 new cases of cervical cancer are registered worldwide annually (Cervical cancer, 2012). The development of the illness can be provoked by the background diseases which lead to the transformation of the vaginal part of the cervix: polyps, papillomas, cervicitis, erosions and others (Badretdinova, Gantsev, & Trubin, 2014). The pathological processes that lead to the transformation of cervical epithelium are regarded as precancerous conditions which can be provoked by the viral infections, such as human papillomaviruses (HPVs), and consequent chronic inflammations. Viral Infection The viral nature of a number of human malignant tumors is proved by clinical research. Recent research data demonstrates that over 90% of cervical cancers contain high-risk HPVs including HPV 16, 18,31, 33, 45 (Bulkmans et al., 2007). All papillomaviruses have similar genetic structure and morphology. They contain three types of capsid proteins and complexes of closed circular DNA with a histone cell (Miller, Puricelli, & Stack, 2012). It is observed that HPV DNA may persist in the cells of the basal layer of epithelium for a significant period, and then it can progress through the inclusion of HPV DNA into the cellular genome and can be developed as the malignant transformation of epithelium (Miller et al., 2012). HPV enters the basal cells of epithelium through micro traumas formed during the sexual contacts. Viral DNA integrates into the cellular nucleus and, while being present in the basal layer in a small number of copies, HPV cannot be detected. During the further HPV expression, the subclinical and clinical stages of the disease commence developing. At this stage, the cytopathic effect of HPV, koilocytosis, occurs in the surface layers of epithelium while the cellular core takes an irregular shape and becomes hyperchromatic due to the accumulation of virion therein (Miller et al., 2012). Despite their high-risk potential, the progression HPV pathogenic effect is conditional. Carriage of HPV shows no malignant process as such, but the risk of cancer development can be increased. Factors that modify the pathogenic effects of HPV and provoke the consequent growth of tumor may include the immune deficiency, other infections, and viruses, or cervical traumas. For example, it is observed that the combination of HIV and HPV increases the risk of malignancy (Isaakidis et al., 2013). The rapid rise of HPV infection occurs among women of 15-25 years old, i.e. after the onset of sexual activity (Bell et al., 2011). The risk factors of infection include the features of reproductive behavior. The research findings make it clear that the number of sexual partners is correlated with HPV infection (Bell et al., 2011). Therefore, the methods for the prevention of HPV infection are the intervention of reproductive behavior and regular clinical examination. For a long time, the only method of HPV detection was the cytological screening based on the identification of cytological transformations of epithelium associated with the infection. However, the results of cytological testing