HPV is a DNA virus, which is resistant to drying, freezing and solvents because it has no envelope, and humans are the only natural hosts of HPV. Currently, there are about 100 types of HPV typing and about 40 types of HPV associated with urinary, anal and reproductive tract infections. According to the risk of HPV causing precancerous lesions and cancer, HPV is divided into low-risk HPV, with at least 12 types, HPV-6 and 11 being the most common, producing condyloma acuminata and cervical intraepithelial neoplasia (CIN) grade I. High-risk HPV: with at least 15 types HPV-16 and 18 are the most common, producing CIN II, CIN III and cervical cancer.
For population-based screening: HPV testing is more suitable for first-line screening; for screening of individuals with financial means: combined HPV and cytology testing is still the best choice; HPV typing is more important than HPV load; HPV 16/18 typing is significant for management of risk stratification
In a study by Dr. Zhao Jian of the Department of Obstetrics and Gynecology at Peking University Hospital, 3086 outpatients with sexual intercourse were screened for HPV positivity at a rate of 63.1%, with low-risk types accounting for 51.4%, high-risk types accounting for 11.7%, and multiple infections accounting for 23.7%. 463 patients had cervical lesions, with an HPV infection rate of 77.3%, including 65% in the cervicitis group; 83.3% in the CIN I group; 95 95 %; CIN III group was 98.1 %. Detection of HPV infection has now become one of the key issues in screening and prevention of cervical cancer. HPV typing is important for clinical CIN screening, evaluation and management of cervical cytologic abnormalities, progression of the disease course, follow-up after CIN treatment, and the epidemiological status of the population and development of viral vaccines.
Dr. Ruan Jianbo’s study showed that in 1206 outpatient high-risk male patients, 28.36% tested positive for HPV, 50.88% for low-risk types and 49.12% for high-risk types. Single infection was 67.54%, secondary infection 21.05%, and multiple 11.4%. High-risk HPV infection may also be closely related to the occurrence of male external genital malignancies, such as Bowen’s disease (squamous carcinoma in situ), penile cancer, anal cancer, etc. Men with high-risk HPV infection as the main type play an important role in the occurrence of cervical cancer in women, and HPV is transmitted to their spouses or regular sexual partners through sexual contact, thus increasing the risk of cervical cancer.
I. Transmission routes
Urinary, anal and genital HPV infection is closely related to sexual intercourse, with a 50% risk of penile-vaginal infection; 10% risk of non-penetrative infection; and 1% risk of no sexual contact, with condom use only partially, but not completely, protecting against genital HPV infection. non-sexual contact transmission includes infection through contaminated daily necessities, etc.; children through perinatal vertical transmission, finger inoculation or self-inoculation, the contaminants, and sexual abuse; and the occurrence of laryngeal papilloma when the fetus passes through the birth canal of an HPV-infected mother during delivery.
Susceptibility factors
The HPV infection has an important relationship with the body’s immune function, especially with the cellular immune function, congenital T-cell function defective people, HIV-positive people, people who received a kidney transplant and low cellular immune function are susceptible to HPV infection. Only 60% of the sexual partners of patients with condyloma acuminata develop the disease, which may have genetic susceptibility factors.
The pathogenesis
The actual process of inoculation is the shedding of epithelium or keratin with viral particles from the diseased party into the epithelial fissures of the healthy party, and the infection occurs.
Fourth, the regression of HPV infection
1, HPV is automatically removed by the body: most people with genital HPV infection is only temporary and lasts about 1 to 2 years.
2, HPV latent infection: that is, HPV virus carriers, HPV virus can be detected on skin mucosa with normal appearance and negative white acetate test. In asymptomatic women, the detection rate of HPV varies widely (2% ~ 44%), after a period of time, some patients disappear, and some patients develop typical condyloma acuminata.
4, HPV clinical infection: by HPV infection caused by the urinary, anal and genital parts of the proliferative damage, visible to the naked eye, including condyloma acuminata, Bowen-like papulosis, giant condyloma acuminata.
5.Precancerous lesions caused by HPV: cervical intraepithelial neoplasia (CIN) is a collective term for a group of precancerous lesions closely related to invasive cervical cancer, which includes cervical atypical hyperplasia and cervical carcinoma in situ. CIN is classified into 3 grades according to the extent of heterotypic cells occupying the epithelial layer of the cervix. CIN grade I means the heterotypic cells are confined to 1/3 of the subepithelial layer; CIN grade II means the heterotypic cells are confined to 1/3 to 2/3 of the subepithelial layer; CIN grade llI means the heterotypic cells are almost or completely involved in the epithelial layer, i.e. severe atypical hyperplasia and carcinoma in situ of the cervix.
The current TBS (The Bethyesa System) classification reflects the progression of cervical disease, and the concept of squamous intraepithelial neoplasia was first introduced. Low squamous intraepithelial lesion (10wersquamous intraepithelial lesion, LSIL): corresponds to histology CIN 1 and CIN2/P16 (-); high squamous intraepithelial lesion (HSIL): corresponds to histology CIN 3 and CIN2/P16(+). Note: P16 (immunohistochemistry) as a biomarker for the diagnosis of cervical precancerous lesions (suggesting biomarkers for E6/E7-driven cell proliferation)
HPV infection is the direct cause of cervical cancer, and cervical cancer is currently the only type of malignancy with a clear cause that can be prevented and cured. The risk of CIN I, CIN II and CIN III developing into cervical cancer is 15%, 30% and 45% respectively.
V. Prevention
1. Condoms: The use of condoms helps reduce the chance of transmission, but it does not mean that transmission will be eliminated. A study of college freshmen found that the annual infection rate of HPV without condoms was 89.3%, compared to 37.8% for users.
2. Cervical cancer.
2006: Merck’s Gardasil (Gardasil), for HPV types 16, 18, 6 and 11 (quadrivalent vaccine), currently approved for use in more than 130 countries worldwide
2007: GlaxoSmithKline’s Cervarix (Huoyancon), for HPV types 16 and 18 (bivalent vaccine)
December 2014: Merck’s nine-valent vaccine (adds 31, 33, 45, 52 and 58)
HPV vaccination is the primary means of prevention, but does not mean that subsequent cervical cancer screening can be dispensed with, as the vaccine does not protect against all high-risk HPV types.
It should be used for boys and girls aged 11 to 12 years, with a catch-up vaccine available by age 26. Three-dose immunization schedule: vaccination at 0th, 1st to 2nd, and 6th months.
VI. Summary
Pay attention to HPV infection, understand the regression of HPV infection, treat HPV infection reasonably, and pay attention to the carcinogenicity of HPV.
Main references
1. Zhu Xuejun, Wang Baoxi, Sun Jianfang, Xiang Leihong, eds. Dermatology. Beijing: Peking University Medical Press, 2011.
2. Zhao Jian, et al. Chinese Journal of Laboratory Medicine, 2006,29(12):1148-1151
3. Ruan Jianbo, et al. Chinese Journal of Dermatologic Venereology, 2012,26(7):617-618