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HUMAN ADDITIONAL VIRUS AND CERVICAL CANCER

Živilė Gudlevičienė

Institute of Oncology, Vilnius University

Printed by: Ž. Gudlevičienė . “Human Papillomavirus and Cervical Cancer.” Health, 2004, 7, 30–32.

 

The role of viruses in the formation of tumors of various localizations is extensively studied. Researchers focus on T-cell leukemia type 1 virus (HTLV-1), herpes viruses (HHV-8 and Epstein-Barr viruses), hepatitis B, and human papilloma viruses (HPV). One common feature common to all these viruses is that they have a very long latency period from the initial infection to the development of cancer. This period varies and can last from 10 to 40 years. The mechanisms of cell malignancy are different, but the essence of all of them is the dysfunction of the genes involved in the control of cell division and growth. Today, it is estimated that about 15 percent of all malignancies are caused by viruses: hepatitis B virus is associated with hepatocellular cancer, both herpes viruses – nasopharyngeal cancer and Burkitt’s lymphoma, herpes > virus type 8 – with Kaposi’s sarcoma. It has been hypothesized that human papillomavirus infection plays an important role in the development of cervical cancer around the 1970s (1).

The results of many studies show that HPV is found in 90 to 100 percent of cases. women with cervical cancer. And only 5-20 percent. healthy women. Therefore, the International Agency for Research on Cancer in Lyon, France, came to the important conclusion that HPV is one of the important factors in the development of cervical cancer. HPV infection in healthy women is highly age-dependent, with young people (20-25 years old) and HPV infection in sexually active individuals ranging from 20 to 80 percent. However, only a small proportion of HPV-infected women, from 3 to 10 percent. (depending on the population) are carriers of the infection. They belong to women at high risk of cancer. It should be noted that viral infections alone are not enough to cause cancer. Environmental pollution, a woman’s hormonal status, immune response, smoking, and other factors influence the existence and expression of this infection (1).

Today, more than 120 types of HPV have been identified that infect skin or mucous membranes . They most commonly cause benign skin papillomas and precancerous lesions and cancer of the cervix.

HPV is divided into several groups: viruses in the high-risk group, moderate and low-risk groups of cancer . HPV 16, 18, 31 or 45 are commonly found in cervical malignancies and are referred to as high-risk cancer types , while HPV 6, 11, 42, 43 or 44 are less common in these tumors, i.e. i> low cancer risk viruses. The moderate risk of cancer includes those types of viruses that are equally common in both cervical and healthy women (2).

HPV infection is transmitted through contact through infected genital or outlet pathways. It has been observed that women whose men had warts on the external genitalia also develop genital warts. HPV infection depends on the number of sexual partners, and increases with the number of partners. In adolescents and young women, the risk of contracting HPV increases with each new partner. Juvenile reversible respiratory papillomatosis (a rare disease) in infants and children suggests that HPV infection can be transmitted to an infant during childbirth. Cases of transmission of HPV through the skin have also been reported. HPV DNA can also be found on medical instruments. Blood-borne infection is not described.

Most individuals who are infected with HPV do not have any complaints that would worry them, and the doctor does not notice any cervical lesions when examining the patient. Only decreased cellular immunity can stimulate the replication of the virus and thus increase the chance of developing new or recurrent cervical lesions. It should be noted that only a small proportion of individuals infected with HPV types at high risk for cancer develop cervical cancer.

As already mentioned, many violations are caused by HPV. Most macroscopically visible warts are caused by low-risk HPV. All reversible respiratory papillomatoses are associated with these viruses. HPVs with a high cancer risk, including HPV types 16 and 18, are most commonly found in cervical specimens and persist for the longest time compared to other HPV types. Significant squamous epithelial lesions (HSIL) caused by high-risk HPV types (HPV 16 or 18) can occur spontaneously, in addition to the initial mild squamous epithelial lesions (LSIL). Most patients with cervical cancer are most commonly infected with HPV types 16 or 18. HPV type 18 is more common (approximately 50%) in cervical adenocarcinoma, mixed carcinoma (glandular and squamous cell carcinoma), and small cell carcinoma than in squamous cell carcinoma. HPV type 16 is the most common (more than 50%) case of the latter disease.

The types of viruses, the variety of factors, and the host immune response determine whether genital HPV infection will eventually disappear, benign cervical mucosal lesions develop, or whether malignant transformation of cancer cells and cancer develop slowly over many years. The length of time an infection is present in the body is highly dependent on the type of virus. HPV type 16 virus can be present in the body for up to 16 months without causing any damage to the cervical mucosa. The infection may later disappear. Other viruses with a high risk of cancer can be in the body for an average of about 8 months, and viruses with a low risk of cancer for about 4-5 months.

Mild cervical mucosal dysplasias are most commonly associated with low- and high-risk types of HPV. Most minor cervical dysplasias regress spontaneously within 3 years and only 15–25%. of which high-grade squamous cell lesion (HSIL) develops within 2-4 years. The risk of progression of cervical mucosal lesions depends on the type of HPV. It has been found that in the case of HPV type 16 infection, changes in squamous epithelial cells from low to large develop significantly faster than in the case of infection with another type of HPV. Other risk factors, such as smoking, hormonal or immune system disorders, also contribute to the above-mentioned high-grade cervical lesions. In the high-risk HPV type, lesions may develop immediately without initial minor changes. In HSIL, HPV types with a high risk of cancer are the most common (about 90% of cases). When HPV DNA enters the host genome, the infection is irreversible. Spontaneous regression of significant squamous epithelial changes is rare, and possibly 33-50%. HSIL lesions progress to invasive cancer if left untreated. However, this process can take many years or decades, making the treatment of precancerous cervical lesions effective and preventing the development of cervical cancer.

The results of research conducted at the Institute of Oncology of Vilnius University show that the incidence of HPV in women with cervical cancer is 92.0%, HPV type 16 predominates; HPV type 18 is less common than in some other countries. The International Agency for Research on Cancer, summarizing data from 9 countries (3), finds that HPV infection in cervical cancer is about 90.7%. HPV infection in healthy women, according to our research – 23.6 percent.

The importance of HPV testing in screening programs for cervical pathology is increasingly debated. Women diagnosed with HPV infection, and in HPV 16 or 18 with a particularly high risk of cancer, should be monitored more closely by a gynecologist according to specially designed schemes.

Studies of the prevalence of HPV and its types in populations are very important in the development of therapeutic and prophylactic vaccines against HPV. Once women’s infection with HPV and its interaction with other factors that cause cervical cancer have been identified, the ground will be prepared for active cancer prevention, including one of the most promising prevention measures – vaccination, for which most countries, including Lithuania, are actively preparing.

Literature:

1.      Bosch FX, Lorincz A, Mu?oz N, Meijer CJLM, Shah KV.  The causal relation between human papillomavirus and cervical cancer.  J Clin Pathol 2002; 55:244-65.

2.      Kisseljov F.L. Virus-associated human tumors: cervical carcinomas and papillomaviruses. Biochemistry, 2000,65(1),68-77.

3.      EUROGIN. Conclusions: cervical cancer control, priorities and new directions. International charter. Paris, April 2003.

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