60% ~ 70% of women have been infected with hpv virus, and people, especially women, have great fear of cervical cancer. In fact, cervical cancer is not terrible. It is the only cancer among all cancers that can be effectively prevented, discovered and treated early. Most women who are afraid of cervical cancer stem from the lack of knowledge about cervical cancer. Modern medicine has confirmed through research that women suffering from cervical cancer are caused by cervical infection with human papillomavirus (HPV). Although there is a correlation between cervical cancer and human papillomavirus, not all women infected with human papillomavirus will develop cervical cancer. Because human papillomavirus widely exists in nature, human skin, digestive tract, respiratory tract and so on all carry this virus. Therefore, it is possible for all women who have sex to bring human papillomavirus into the reproductive tract through sexual contact. Medical workers have conducted a general survey of women aged 18 ~ 28, and found that human papillomavirus infection is not uncommon. Experts speculate that as far as women are concerned, the cumulative lifetime infection rate of hpv can be as high as 60% ~ 70%. In other words, 60% ~ 70% of women are infected with human papillomavirus in their lifetime, but this infection is usually short-lived. Because when the human body is infected with this virus, the body will gradually, and a few patients will soon form immunity to the virus. When the immunity is strong enough, human papillomavirus will be eliminated. Therefore, a large number of medical statistics show that although the proportion of human papillomavirus infection is very large, most of them are transient, that is, the virus will naturally disappear within 1-2 years (generally referring to human papillomavirus infection). Most women's immune system can eliminate the human papillomavirus entering the body, and only a few women with weak immune function can't eliminate the human papillomavirus entering the body, which leads to the continuous infection of human papillomavirus, but this process takes about 8 ~ 12 years to develop into cervical cancer. Almost all patients with cervical cancer found in clinic are women over 30 years old. Therefore, women who have sex can start HPV -DNA testing after the age of 30. The test result is negative, indicating that there is no human papillomavirus infection, so there is no risk of cervical cancer for a long time. So this examination can be done once every three years. If the test result is positive, it may not necessarily develop into cervical cancer, because the immune system in the body may destroy the virus. It is possible to develop cervical cancer. So we should do a cervical smear first to see if there are any abnormal cervical cells at present. Otherwise, these two inspections should be reviewed once a year. Once an abnormality is found, it can be treated immediately to nip cervical cancer in the bud. Therefore, as far as women are concerned, hpv infection has a strong universality and self-limitation. Even if you are infected with human papillomavirus, there is nothing to be afraid of. Usually, the human body can be gradually removed. Women with poor immunity can completely avoid the occurrence of cervical cancer by doing regular gynecological examination and cancer screening once a year. Human papillomavirus (HPV) is a highly specific epithelial virus. For a long time, it has been known that human papillomavirus can cause human benign tumors and warts, such as human common warts, condyloma acuminatum and papilloma, which grow on the mucosa near reproductive organs. Human papillomavirus (HPV) is a species-specific epithelial virus, which belongs to a small DNA virus with double-stranded closed loop and contains about 8000 base pairs. It includes 8 early open reading frames (E 1-E8), 2 late reading frames and 1 non-coding long control regions. In the early open reading framework, E6 and E7 genes are the most important genes to stimulate cell growth, and E6 and E7 proteins encoded by E6 and E7 lead to the immortalization of cervical epithelial cells. The late reading frame L 1 and L2 genes encode the major and minor capsid proteins of human papillomavirus, respectively, and are assembled into the capsid of human papillomavirus. Since 1976 zur Hansen put forward that human papillomavirus may be the carcinogen of sexually transmitted diseases, the study on the relationship between human papillomavirus infection and cervical cancer has become a hot topic in the etiology of tumor virus. There is no special drug treatment for human papillomavirus. In fact, there is no medicine to treat the virus. Interferon, etc. all improve immunity and do not directly correspond to viruses. Human papillomavirus is easy to spread, but human papillomavirus does not mean cancer. In particular, the appearance of human papillomavirus antibodies in blood can only indicate that human papillomavirus has been infected, while most people will heal themselves within one or two years if human papillomavirus is found in secretions or cervical shedding. Sexually transmitted diseases are generally considered to be sexual contact infections, or contact with secretions (including sweat) of sexually transmitted diseases, and are not transmitted through the air. This is because people's resistance is limited, and too strong an invasion may not be able to resist, nor does it mean that all viruses can cause disease. Commonly known as "cauliflower", venereal warts are caused by human papillomavirus infection, and women may suffer from cervical cancer after warts occur. Three steps, human papillomavirus infection-self-healing or developing into warts or concealment-long-term infection increased. After all, in addition to life, women also want to maintain normal functions, treat them early, have little damage, and cannot affect their lives. At the same time, it should be pointed out that it is not the cause of sexual life-human papillomavirus-cervical cancer, but unmarried women may also suffer from cervical cancer, of course, the probability will be much smaller. Of course, some people use this as an argument. Coburn, an American obstetrician and Congressman, thinks that human papillomavirus is another AIDS crisis. He suggested that condoms should be listed on the package to show that the product can't prevent human papillomavirus and let women know that condoms can't resist the virus that can cause cervical cancer. As a virus, especially a widely spread virus, human papillomavirus should have special disinfection and prevention procedures to ensure that condoms can prevent the spread of the virus. Simply put, soaking tap water (chlorinated) for one night, basking in the sun during the day and using it at night is absolutely anti-HPV. However, if you have time, you'd better eat well, exercise more, rest more, have better immunity, and be less susceptible to human papillomavirus infection. Human papillomavirus is the general name of a group of viruses, belonging to a family. Viruses are similar in morphology, but the DNA restriction endonuclease patterns are different, and the antigenicity of core-shell proteins is different. The result under the electron microscope is shown in figure 1. At present, there are about 80 kinds of human papillomavirus, which can be divided into skin-type human papillomavirus and genital epithelial human papillomavirus according to the location of infected epithelium. About 35 types can infect the female reproductive tract, and about 20 types are related to tumors (the human papillomavirus infections mentioned below are all female reproductive tract infections). According to the different types of human papillomavirus and the risk of tumor occurrence, it can be divided into low-risk and high-risk human papillomavirus. The low-risk types of human papillomavirus are HPV6, 1 1, 42, 43, 44, etc. It often causes benign lesions such as external genital condyloma, including cervical intraepithelial low-grade lesions (CIN I). High-risk human papillomavirus includes HPV 16, 18, 3 1, 33, 35, 39, 45, 5 1, 52, 56, 58, 59, 68, etc. It is related to cervical cancer and cervical intraepithelial lesions (CIN II/III). 2. Study on the Prevalence of Human Papillomavirus Infection in Female Genital Tract Regarding the prevalence of human Papillomavirus infection, the positive rate of human Papillomavirus infection reported in each study is different due to the differences in the source of test samples, the detection technology of human Papillomavirus used, the detection type of human Papillomavirus and the population in the study area. The infection rate determined by detecting human papillomavirus DNA is slightly higher, but the infection rate determined by cytology or colposcopy is very low. The infection rate was about 10-20% by various direct detection methods such as in situ hybridization or dot blot hybridization, and the PCR detection result was higher. Female college students in a university (97% have had sexual relations, with an average of 4 sexual partners) were examined. The results showed that the detection rate of PCR was 46%, while the detection rate of dot blot hybridization was only 1 1%. It can be seen that the detection method affects the detection of human papillomavirus infection. In melkert's experiment. It is 4.65438 0% in ordinary women. Herrero reported that the infection rate of human papillomavirus among women aged 65,438+08-94 in rural Costa Rica was 65,438+06%. At present, many studies use HC method to detect human papillomavirus DNA, because HC method is more sensitive, so the detection rate is higher. Clavel C et al. used HC-II method to detect human papillomavirus infection in women aged 1, 5 18 15-72, and found that the positive rate of human papillomavirus infection was 22.3%. 3. Age distribution The infection rate of human papillomavirus mainly depends on the age and sexual habits of the population. Many studies have found that the infection rate of human papillomavirus is the highest among sexually active young women, and the peak age is 18-28 years old, and the infection rate decreases obviously with the increase of age, but most data reports do not distinguish between high-risk and low-risk types, as shown in Figure 2. Most human papillomavirus infections can disappear in a short time, and the virus is gradually eliminated by the body through the autoimmune system, especially the low-risk human papillomavirus is more easily eliminated by the body, lasting about 18 months, so the positive rate of low-risk human papillomavirus infection shows a downward trend. However, for high-risk human papillomavirus infection, many studies report that the peak age of infection is 20-30 years old. At this stage, the infection rate is temporary and can reach 25-30%. After that, the infection rate gradually decreased, and after 35 years old, 5- 10% was in a state of continuous infection with high-risk human papillomavirus. There is still some controversy about whether the positive rate of human papillomavirus infection begins to rise or fall after 40 years old, and more detailed data is needed to verify it. 4. Epidemiological factors of human papillomavirus infection Because human papillomavirus infection usually has no obvious clinical symptoms, its detection rate varies with various methods, and it is difficult to determine the epidemiological factors of human papillomavirus infection. However, it is obvious that human papillomavirus infection is a sexually transmitted disease, which is related to sexual behavior factors. However, good personal hygiene, attention to menstrual hygiene, hygiene before and after the same room, and the use of intrauterine devices can reduce the probability of human papillomavirus infection. (1) Sexual behavior: Most studies show that the number of women's recent sexual partners, the frequency of sexual intercourse and their genital warts are closely related to human papillomavirus infection. Although studies have shown that the age of first sexual intercourse is also related to human papillomavirus infection, this factor is affected by the number of sexual partners, and the risk is not significant after adjusting the number of sexual partners. (2) Immune factors: Host immunity plays an important role in the progress of human papillomavirus infection and pathological changes. It was found that the infection rate of human papillomavirus in immunosuppressants after renal transplantation was 17 times that of normal people. The infection rate of human papillomavirus among HIV-infected people has also increased. Due to the chaotic sexual behavior of HIV-infected people, a large number of sexual partners and the younger age of their first sexual behavior, the probability of human papillomavirus infection has increased. However, some studies cannot prove that there is a direct correlation between immunosuppression and human papillomavirus infection. Because of the high risk of self-exposure or the reduced ability of the body to resist latent virus, the HIV population may increase the infection rate of human papillomavirus. The detection level of HPV DNA in this population is higher than that in the normal population, indicating that the ability of the body to inhibit HPV infection is reduced. (3) Pregnancy: Studies show that the number of pregnant women, the number of deliveries and the number of miscarriages will not increase the risk of human papillomavirus infection, but the number of teratomas is related to human papillomavirus infection. Studies have shown that the infection rate of human papillomavirus in pregnant women is high, and the amount of virus detected also increases, but this may be due to the increase of virus level during pregnancy, which improves the detection efficiency. A study of detecting human papillomavirus by PCR confirmed this view. The detection of human papillomavirus by PCR has nothing to do with the virus content, and there is no significant difference in infection rate between pregnant women and non-pregnant women (9.6%/ 10.9%). (4) Oral contraceptives: Although oral contraceptives will increase the risk of cervical cancer, it is still controversial whether it affects human papillomavirus infection. Studies have shown that oral contraceptives do increase the probability of human papillomavirus infection, but some people think that oral contraceptives have no effect on the occurrence of low-grade cervical lesions, but will increase the risk of high-grade cervical lesions. Therefore, oral contraceptives are considered to change the course of the disease rather than directly affect the infection rate of human papillomavirus. 5. The risk of HPV infection and cervical cancer The relationship between HPV infection and cervical cancer was first put forward in 1970s. Since then, many epidemiological and molecular studies have undoubtedly confirmed the etiological relationship between human papillomavirus and cervical cancer. Bosch and Manos collected cervical cancer biopsy samples from 22 countries for PCR detection, and found that human papillomavirus DNA could be detected in 99.7% of tumors, with no significant difference among countries. This is the highest detection rate of human tumor pathogenic factors reported so far, and it also shows that the correlation between human papillomavirus infection and cervical cancer is of universal significance. Case-control study is an analytical epidemiological method to test the hypothesis of etiology. No matter the large-scale epidemiological study in Latin America with low accuracy detection technology (FISH) or the study with high sensitivity detection technology (PCR, HC-II), all the results show that there is a significant correlation between human papillomavirus infection and cervical cancer (OR=3.6-254.2), especially human papillomavirus HPV 16 and 18. A population-based case-control study conducted by Muňoz et al. in Colombia and Spain (the incidence of cervical cancer in the former is 8 times higher than that in the latter) included 436 histologically confirmed cases and 387 randomly selected cases as controls, and three HPV DNA detection techniques (ViraPap, SH and PCR) were used at the same time. In this study, the selective bias of population and region was avoided, and the differences between detection technologies were considered. After adjusting for some confounding factors, the three detection methods reached the same conclusion: HPV 16, 18, 3 1, 33 and 35 were strongly correlated with cervical cancer in two countries, suggesting that HPV and cervical cancer have etiological links. Cohort study is another important analytical epidemiological method to verify the hypothesis of disease etiology, which can directly reflect the time series of human papillomavirus infection and cervical cancer, and more effectively verify the hypothesis of disease etiology. Campion followed up 100 cases of mild cervical intraepithelial lesion (CINⅰ Ⅰ) for more than two years. 56% of HPV 16 and 18 positive patients progressed to severe cervical intraepithelial lesion (CINⅲ Ⅲ), while only 20% of HPV6 positive patients progressed. Murthy and other studies showed that 63 cases of cervical atypical hyperplasia developed into carcinoma in situ, and the positive rate of HPV1618 was 68.3%, while the positive rate of 44 cases of non-progressive atypical hyperplasia was 27.3%, with a relative risk of 5.9 (95% CI: 2.5-65438). In addition, strong evidence of human papillomavirus carcinogenesis has been obtained in cytology and molecular biology. 1995 who and IARC have determined that human papillomavirus is the cause of cervical cancer. 6. The most common HPV types of human papillomavirus type and cervical cancer reproductive tract infection are 16,18,6, 1 1. HPV6 type and 1 1 type often infect vulva, anus, vagina and other parts, belonging to low-risk type, which are more common in female condyloma acuminatum or low-grade cervical intraepithelial lesions, and have no obvious relationship with cervical invasive cancer; However, 16 and 18 are high-risk types. The study of cervical cancer tissue samples around the world found that HPV 16 and 18 had the highest infection rates. Among all the detected types, HPV 16 accounts for 50%, HPV 18 accounts for 14%, HPV45 accounts for 8%, HPV3 1 accounts for 5%, and others account for 5%. The types of human papillomavirus are related to the pathological types of cervical cancer. HPV 16 is the main type of cervical squamous cell carcinoma (5 1% squamous cell carcinoma), and HPV 18 is the main type of cervical adenosquamous carcinoma (56% adenosquamous carcinoma) and cervical adenosquamous carcinoma (39% adenosquamous carcinoma). HPV 16 and 18 are very common, and there is no obvious regional difference. Some types of human papillomavirus have geographical differences. The detection rate of HPV infection in China 52 and 58 is high. A study conducted in Taiwan Province Province also showed that types 52 and 58 were more common. Human papillomavirus type 45 is very common in cervical cancer tissues in West Africa, while human papillomavirus types 39 and 59 only appear in cervical cancer tissues in Central America and South America. 7. The role of human papillomavirus infection in the natural history of cervical cancer. Genital tract human papillomavirus infection is a long-term process, which can lurk in cells for several years. Once the human immunity is reduced, the latent virus can resume its activities. The process of human papillomavirus infection is usually divided into latent infection stage, subclinical infection stage, clinical symptom stage and human papillomavirus-related tumor stage. Cervical cancer also has a series of precursor lesions, namely atypical hyperplasia of cervical epithelium, which is pathologically called cervical intraepithelial neoplasia (CIN). Generally, it is divided into three grades according to the severity: mild cervical intraepithelial neoplasia (CIN grade ⅰ), moderate cervical intraepithelial neoplasia (CIN grade ⅱ) and high cervical intraepithelial neoplasia (CIN grade ⅲ). All these precancerous lesions may develop into invasive cervical cancer. Under some natural or experimental conditions, papilloma induced by human papillomavirus often turns into squamous cell carcinoma, but not all people infected with human papillomavirus and CIN will develop into cancer. For most papillomas, this transformation also needs the existence of other auxiliary factors, such as smoking, chemicals, host factors (such as HIV infection), environmental synergy factors, etc., all of which can induce and start the transformation of warts and papillomas into malignant tumors. Some scholars have put forward the hypothesis that human papillomavirus and HSV cooperate to induce cervical sub-transformation: specific papillomavirus infects normal cells, leading to the proliferation of papilloma cells, and under the initiation of HSV infection, it causes malignant transformation of cervical epidermis, eventually leading to invasive cancer. This hypothesis needs further verification. There are many studies on human papillomavirus infection and CIN results. Some prospective studies showed that 15-28% of women infected with human papillomavirus developed into cervical squamous intraepithelial lesions (SIL) within two years, especially human papillomavirus 16 and 18 types. Whether HPV positive women can develop cervical intraepithelial lesions and cancer is closely related to the type of HPV. Studies have shown that among women with low-grade cervical lesions, women with high-risk human papillomavirus infection are at greater risk of cervical lesions than women with low-risk human papillomavirus infection or negative human papillomavirus. In addition, the dose level of human papillomavirus DNA and the time of first infection with human papillomavirus are also important. Here, two years is an important concept of time, and the contest between human immune system and human papillomavirus will be known within two years. 8. In short, genital human papillomavirus infection is a common sexually transmitted disease. 50% of sexually active women may be infected with at least one human papillomavirus. Because HPV infection is the cause of cervical cancer, we must attach importance to this infection, strengthen the development of HPV vaccine and eliminate its harm to human beings.