What Are the Effects of HPV on Pregnancy?

This disease is also known as genital warts, genital warts, or venereal warts. It is a sexually transmitted disease caused by human papillomavirus (HPV) infection. There are many types of HPV. The main types of HPV are HPV 1, 2, 6, 11, 16, 18, 31, 33, and 35. Among them, long-term HPV 16 and 18 infection may be related to the occurrence of cervical cancer in women.

HPV-lgG antibody

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This disease is also called condyloma acuminatum,

HPV is a group

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The HPV infection rate mainly depends on the age and sexual behavior of the population. Many studies have found that sexually active young women have the highest HPV infection rates, with peak ages ranging from 18 to 28 years, and a significant decline with age, but most data reports do not distinguish between high-risk and low-risk types, as shown in Figure 2. Most HPV infections can disappear in a short period of time. The body gradually clears the virus through the autoimmune system, especially the low-risk type HPV is more easily cleared by the body, which lasts about 18 months, so the positive rate of low-risk HPV infection Showing a downward trend. However, for high-risk HPV infections, many studies have reported that the peak age of infection is 20-30 years. At this stage, the infection is temporary and the infection rate is high, which can reach 25-30%. After that, the infection rate has gradually decreased, and 35 years old. The last 5-10% were persistently infected with high-risk HPV. There is some controversy as to whether the positive rate of HPV infection begins to rise or fall after the age of 40, and more detailed data are needed to verify it.

Because HPV infection usually has no obvious clinical symptoms, and its detection rate varies by various methods, it is difficult to determine the epidemic factors of HPV infection. However, it is clear that HPV infection is a sexually transmitted disease and is related to sexual behavioral factors. The individual's health status is good, pay attention to menstrual hygiene, sanitation before and after the same room, use of intrauterine contraceptive rings, etc. can reduce the risk of HPV infection.

(1) Sexuality: Most studies have shown that the number of recent sexual partners, the frequency of sexual intercourse, and the genital warts of sexual partners are all closely related to HPV infection. Although some studies have shown that the age of first sexual intercourse is also related to HPV infection, this factor is affected by the number of sexual partners. After adjusting the number of sexual partners, the risk is not significant.

(2) Immune factors: The host's immunity has a great effect on the progress of HPV infection and disease. Studies have found that the rate of HPV infection in immunosuppressed patients with kidney transplantation is 17 times that of the normal population. HPV infection rates are also increasing in HIV-infected people. Due to the chaotic sexual behavior of HIV-infected people, the number of partners, and the age of first sexual intercourse, etc., make the chance of HPV infection increase. However, some studies have not proved that immunosuppression is directly related to HPV infection. The HIV population may have an increased HPV infection rate due to a high risk of self-exposure or a reduced ability to resist latent viruses. HPV DNA detection in this population The level is higher than the normal population, which indicates that the body's ability to suppress HPV infection is reduced.

(3) Pregnancy: Studies have shown that the increased number of pregnancies, the number of childbirths, and the number of miscarriages do not increase the risk of HPV infection. Some studies have shown that HPV infection rates are higher in pregnant women and that the amount of virus detected is higher, but this may be due to the increased detection efficiency of virus during pregnancy. A study using HPV to test HPV confirmed this view. PCR testing for HPV virus-independent virus content found no significant difference in infection rates among pregnant and non-pregnant women (9.6% / 10.9%).

(4) Oral contraceptives: Although oral

1. Unclean sexual history.

2. Typical skin lesions are pimples on wet parts such as the genitals or perianal area, nipple-like, cauliflower-like, or chicken coronal fleshy neoplasms with rough, keratinized surfaces.

3 Acetic acid white test was positive, pathological sections showed poor keratosis and concave cells.

4 Nucleic acid hybridization can detect HPV-DNA related sequences, and PCR detection shows specific HPV-DNA amplification bands.

And the risk of cervical cancer

The relationship between HPV infection and cervical cancer was first proposed in the 1870s. Since then, many epidemiological and molecular studies have undoubtedly confirmed the etiology of HPV and cervical cancer. Bosch and Manos et al. Collected cervical cancer biopsy specimens from 22 countries for PCR detection and found that HPV DNA can be detected in 99.7% of tumors, and there is no significant difference between countries. This is the highest detection percentage of human tumorigenic factors reported to date, and it indicates that the correlation between HPV infection and cervical cancer is of universal significance.

A case-control study is an analytical epidemiological method to test the etiology hypothesis. Whether it is a large-scale epidemiological study using less accurate detection technology (FISH) in Latin America or a study using more sensitive detection technology (PCR, HC-II), all results show that HPV infection and Cervical cancer has a significant correlation (OR = 3.6-254.2), especially HPV 16 and 18 types. Muoz et al.'S case-control study based on populations in Colombia and Spain (the former had an eight-fold higher incidence of cervical cancer than the latter) included 436 histologically confirmed cases and randomly selected 387 cases from the population In contrast, three HPV DNA detection technologies (ViraPap, SH, and PCR) were used simultaneously. This study avoided selective shifts in populations and regions, while taking into account differences in detection techniques. After adjusting for some confounding factors, the three detection methods all reached the same conclusion: HPV16, 18 in two countries. Types 31, 33, and 35 are strongly correlated with cervical cancer, suggesting that HPV has a causal relationship with cervical cancer. The cohort study is another important epidemiological method used to verify the disease etiology hypothesis. It can directly reflect the chronology of HPV infection and cervical cancer occurrence, and more effectively verify the etiology hypothesis. Campion followed 100 cases of mild cervical intraepithelial lesions (CIN I) for more than two years. 56% of HPV16 and 18 positive patients progressed to severe cervical epithelial lesions (CIN III), while only 20% of HPV6 positive subjects progressed . Murthy et al.'S study using in situ hybridization showed that 63 cases of cervical atypical hyperplasia developed into carcinoma in situ. The positive rate of HPV16 / 18 was 68.3% in tissue specimens, while 44 cases of non-proliferative atypical hyperplasia had a positive rate. 27.3%, the relative risk was 5.9 (95% CI: 2.5-14.1), which has significant statistical significance. In addition, strong evidence of human papilloma virus carcinogenesis has been obtained in cytology and molecular biology. In 1995, WHO and IARC identified HPV as the cause of cervical cancer.

HPV type and cervical cancer

The most common types of HPV in genital tract infections are types 16, 18, 6, and 11. HPV6 and 11 types often infect the vulva, anus, vagina and other parts. They belong to the low-risk type. They are common in women with genital warts or low-grade cervical intraepithelial lesions, and they are not significantly associated with invasive cervical cancer. Types 16 and 18 are high-risk types. do not. Studies of cervical cancer tissue specimens from countries around the world have found that HPV16 and 18 types have the highest infection rates. Among all types detected, HPV16 accounts for 50%, HPV18 accounts for 14%, HPV45 accounts for 8%, HPV31 accounts for 5%, and others Type of HPV accounts for 23%. The type of HPV is related to the pathological type of cervical cancer. HPV16 predominates in cervical squamous cell carcinoma (51% of squamous cell carcinoma specimens), and in cervical adenoid epithelial cell carcinoma (56% adenoid epithelium) Cell carcinoma specimens) and cervical adenosquamous cell carcinoma (39% adenosquamous carcinoma specimens) HPV18 predominates. HPV16 and 18 infections are common and there are no obvious regional differences. Some HPV types have geographical differences. The detection rates of types 52 and 58 among HPV infection types in China are high. A study in Taiwan also showed that types 52 and 58 are more common. HPV45 is common in cervical cancer tissues in western Africa, while HPV39 and 59 are only found in cervical cancer tissues in central and southern America.

Role in the natural history of cervical cancer

HPV infection of the reproductive tract is a long-term process that can lie in the cell for several years. Once the body's immunity is reduced, the latent virus can resume its activity. The HPV infection process is usually divided into a latent infection period, a subclinical infection period, a clinical symptom period, and an HPV-related tumor period. Cervical cancer also has a series of precursor lesions, that is, atypical hyperplasia of the cervical epithelium, which is called pathologically cervical intraepithelial neoplasia (CIN), which is usually divided into three levels according to severity: cervical intraepithelial mild neoplasia (CIN I), Cervical intraepithelial moderate neoplasia (CIN II) and cervical intraepithelial high neoplasia (CIN III), these precancerous lesions may develop into invasive cervical cancer.

Under certain natural or experimental conditions, although HPV virus-induced papilloma has a tendency to transform into squamous cell carcinoma, not all HPV-infected persons and CIN will progress to cancer. For most papillomas, this transformation also requires the presence of other cofactors, such as smoking, chemicals, host factors (such as HIV infection), and environmental synergistic factors, all of which cause mutagenesis of warts and papilloma into malignant tumors And start-up. Some scholars have proposed the hypothesis that the synergistic effect of HPV and HSV induces cervical subtransformation: specific papilloma virus infection of normal cells leads to papilloma cell proliferation. Under the initiation of HSV infection, malignant transformation of the cervical epidermis occurs. Causes invasive cancer. This hypothesis needs further verification.

Human papillomavirus (HPV) is an epithelial virus with high specificity. For a long time, HPV has been known to cause benign tumors and warts in humans, such as growing on the skin and mucous membranes near the reproductive organs. Human warts, condyloma acuminatum, and papilloma growing on the mucous membranes. HPV is a species-specific epithelial virus, a double-stranded closed-loop small DNA virus that contains approximately 8,000 base pairs. These include 8 early open reading frames (E1-E8), 2 late reading frames, and a non-coding long control area. In the early open reading frame, E6 and E7 genes are most important for cell growth stimulation, and E6 and E7 proteins encoded by E6 and E7 cause immortalization of cervical epithelial cells. The L1 and L2 genes in the late reading frames encode the major and minor capsid proteins of HPV, respectively, and assemble into HPV capsids. Since zur Hansen proposed that HPV may be a cause of sexually transmitted cancer in 1976, the research on the relationship between HPV infection and cervical cancer has become a hot topic in the study of the cause of tumor virus.

There are many studies on HPV infection and outcome of CIN subjects. Some prospective studies have shown that 15-28% of HPV-positive women progress to cervical squamous intraepithelial lesions (SIL) within 2 years, and HPV 16 and 18 infections are particularly at risk. Whether HPV-positive women can progress to high levels of cervical intraepithelial lesions and cancer is strongly related to the type of HPV. Studies have shown that among women with low-grade cervical lesions, women with high-risk HPV infection are more at risk of developing cervical lesions than women with low-risk HPV infection or HPV-negative women. In addition, the HPV DNA dose level and the time of first HPV infection are also important. Here, two years is an important concept of time. The battle between the human immune system and HPV is clear within two years.