1. The old man Born in 1936, German medical scientist and virologist Harald zur Hausen.
Harald has been working on the relationship and mechanism between human papillomavirus (HPV) and cervical cancer since 1970. The results proved that – there is a strong relationship between the two and that certain types of
HPV is the causative agent of cervical cancer. 2. HPV high-risk genotypes vs. low-risk genotypes High-risk types (12): 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, cause more than 90% of cervical lesions above CIN grade II – persistent infection with high-risk types is the main cause of cervical cancer. Suspected high-risk types (8): 26, 53, 66, 67, 68, 70, 73, 82. Low-risk types (11): 6, 11, 40, 42, 43, 44, 54, 61, 72, 81, 89, which mainly cause wart-like lesions and CIN, and cause cervical cancer at less than 5%. HPV vaccine is the first human attempt to eradicate a type of cancer through a vaccine, which is of epoch-making significance. The current HPV vaccine prevents high-risk HPV types, with 16 and 18 being the most potent (causing about 70% of cervical cancers). In 2006, the first HPV quadrivalent vaccine approved by FDA was marketed in the United States, and two other vaccines were approved afterwards; in July 2016, China CFDA approved the marketing license of GSK’s bivalent vaccine, all of which cover HPV 16 and 18. 3. From HPV infection to cervical cancer through quadruple play Quadruple play: HPV infection → persistent viral infection causing cervical epithelial cytopathy → persistent viral infection causing cervical precancerous lesions → cervical invasive cancer; the whole process takes about 25-30 years, which is a long process from quantitative to qualitative and gradual to mutational changes. Note here that persistent HPV infection is necessary for cervical lesions to develop into CIN II-III or even cervical cancer. HPV infection alone does not necessarily lead to cervical cancer. In addition, case-control and cohort studies of women with persistent high-risk HPV infection have found a higher incidence of cervical cancer in women who smoke. 4.9 cancers are strongly associated with HPV infection High-risk HPV induces not only cervical cancer but also other cancers. A molecular epidemiological survey in the United States showed that the presence of high-risk HPV type DNA can be detected in the following 9 cancers, especially in cervical carcinoma in situ, anal cancer and cervical cancer
genes in cervical cancer in situ, anal cancer and cervical cancer are more than 90% distributed. 5. HPV vaccine can prevent oropharyngeal cancer Professor Bhisham Chera, a radiation oncologist at the University of North Carolina School of Medicine, conducted a randomized clinical trial, which showed that the detection rate of HPV in the throat of girls who received HPV vaccine was higher than that of unvaccinated girls 4 years later.
The HPV vaccine reduced the incidence of oropharyngeal cancer by significantly lowering the detection rate of HPV compared to unvaccinated girls. 6. How long can HPV vaccination protect against HPV? HPV-associated cancers tend to occur in the first 10-15 years after the onset of sexual intercourse, and if HPV vaccination is administered 5 years before the median sexual intercourse, the protection lasts for about 20 years to achieve maximum effectiveness.
If HPV vaccination is administered 5 years prior to the median sexual initiation, protection will last for about 20 years to achieve maximum effectiveness. Available evidence suggests that experimental monovalent HPV16, 2vHPV, and 4vHPV
vaccines induce a sustained immune response with higher antibody titers than those induced by natural infection, thus preventing infection for at least 8 to 9 years, and possibly longer because there is no unlimited follow-up. Australia was the first country to implement government-funded HPV vaccination, with the national school-based 4vHPV vaccination for females aged 12-13 years launched in April 2007.
In July 2007, a catch-up 4vHPV vaccine was given to females aged 14 to 26 years, and from 2013, routine vaccination was given to males aged 12 to 13 years, with a two-year catch-up for males aged 14 to 15 years. Since then, Australia has seen a significant decline in HPV infections and related diseases, making it a model for HPV vaccination to rapidly reduce HPV-related disease burden in the general population. If HPV vaccination is fully implemented, a significant decline in cervical cancer incidence will occur in approximately 20 years. The 2012 ACS/ASCCP/ASCP guidelines for cervical cancer prevention and early diagnosis screening recommend the following screening process: <21 years of age, no screening, 21-29 years of age, every 3 years Cytology.