The dangers of high-risk human papillomavirus infection

Many people do not have enough knowledge about high-risk human papillomavirus infection, and do not even know how harmful it is. However, through the following introduction, I believe everyone has some understanding of high-risk human papillomavirus infection. In fact, the key to curing the disease is to find out the causes and dangers of the disease so that everyone can take precautions.

High-risk human papillomavirus infection refers to the most common types of HPV infection in the reproductive tract, namely types 16, 18, 6, and 11. HPV types 6 and 11 often infect the vulva, anus, vagina and other parts of the body. They are low-risk types and are more common in women with condyloma or low-grade cervical intraepithelial lesions. They have no obvious association with invasive cervical cancer. Types 16 and 18 are high-risk types.

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 etiological link between HPV and cervical cancer. Bosch, Manos and others collected cervical cancer biopsy specimens from 22 countries for PCR testing and found that HPV DNA could be detected in 99.7% of tumors, with no significant differences between countries. This is the highest detection percentage of human tumor pathogens reported so far, and it also shows that the relationship between HPV infection and cervical cancer is of universal significance.

Case-control studies are an analytical epidemiological method for testing causal hypotheses. Whether it is a large-scale epidemiological study in Latin America using less accurate detection technology (FISH) or a study using more sensitive detection technology (PCR, HC-II), all results show that HPV infection is significantly associated with cervical cancer (OR=3.6-254.2), especially HPV types 16 and 18. In a population-based case-control study conducted by Muňoz et al. in Colombia and Spain (where the incidence of cervical cancer is 8 times higher), 436 histologically confirmed cases and 387 randomly selected controls from the population where the cases were located were included. Three HPV DNA detection techniques (ViraPap, SH, and PCR) were used simultaneously.

This study avoided selective bias in population and region, while taking into account the differences between detection technologies. After adjusting for some confounding factors, the three detection methods reached the same conclusion: HPV16, 18, 31, 33 and 35 were strongly correlated with cervical cancer in both countries, suggesting that HPV and cervical cancer have a causal relationship. Cohort study is another important analytical epidemiological method used to verify the disease etiology hypothesis. It can directly reflect the temporal relationship between HPV infection and cervical cancer, and more effectively verify the etiology hypothesis. Campion followed up 100 cases of mild cervical intraepithelial lesions (CIN I) for more than two years. 56% of those who were HPV16 and 18 positive progressed to severe cervical intraepithelial lesions (CIN III), while only 20% of those who were HPV6 positive progressed. A study by Murthy et al. using in situ hybridization showed that 63 cases of cervical atypical hyperplasia developed into carcinoma in situ. The positive rate of HPV16/18 in tissue specimens was 68.3%, while the positive rate of 44 cases of non-progressive atypical hyperplasia was 27.3%. The relative risk was 5.9 (95% CI: 2.5-14.1), which was statistically significant.

In fact, in 1995, WHO and IARC identified HPV as the cause of cervical cancer. It is important to correctly understand the dangers of diseases such as high-risk human papillomavirus infection and then receive correct treatment. Only with correct treatment can the harm of the disease be eliminated. The impact of the disease will be reduced. Therefore, people must first seek treatment, and go to the hospital for treatment in time after the disease occurs.