The largest HPV16 genome-wide study to date has found a conserved oncoprotein
Guide
The report published on Cell on September 7th is the largest study of the HPV16 genome to date. The study pointed out that HPV16 E7 protein is unchanged in cervical cancer, and it is recommended that researchers should redouble their efforts in developing drugs that block E7 protein.
Human papillomavirus HPV16 accounts for about half of all cervical cancers, but researchers reported on Cell on September 7 found that not all infections were average. HPV16 genomic analysis of 5,570 human cell and tissue samples revealed that the virus is actually composed of thousands of unique genomes, which allows infected women living in the same area to have different HPV16 sequences and cancer risks. Precancerous lesions or cancer-bearing women mostly have a specific version of the viral gene E7, which is a target of interest to researchers.
HPV16 Whole Genome Research to date
Almost all cases of cervical cancer can be attributed to a persistent infection with high-risk HPV, especially HPV16. However, it is unclear why HPV16 poses a greater risk of cancer than other types of HPV infection. Understanding the unique carcinogenic mechanisms of HPV16 is useful for prevention and individualized treatment. Lisa Mirabello, the first author of the National Cancer Institute, pointed out that HPV16 E7 protein is unchanged in cervical cancer. It is recommended that researchers should redouble their efforts in developing drugs that block E7 protein.
The article, published in Cell, performs a genome-wide analysis of 5,570 HPV16-infected cells and tissue samples from women around the world to identify associations between HPV16 gene variants and cervical precancerous lesions and cancer risk. This is the largest study of the HPV16 genome to date. It has increased by an order of magnitude in the number of HPV16 genome studies and is the first large-scale study to evaluate the relationship between HPV16 genome levels and cancer development.
Viral genome diversity and conservation of oncogenic proteins
It is worth noting that the vast majority of HPV16 sequences analyzed are unique to each infected woman. In each woman, the HPV 16 virus has the same genetic sequence at multiple sites. HPV16 has an unexpected diversity in infected women, showing the mechanism by which the HPV16 genome reuses host cells and the fact that it is slowly mutated. This has important clinical implications for HPV transmission patterns, viral clearance and persistence.
In addition, the HPV16 genome significantly reduced variability in patients with cancer and precancerous lesions compared with the benign infection control group. When the researchers focused their analysis on the oncogenic E7 gene, the results suggest that the only potential carcinogenicity of HPV16 stems from the exact form of the E7 protein: E7 is the same worldwide. In order for cancer to form, it must be conservative. Any change seems to take away its ability to cause cancer.
Research significance and future research direction
In future research, in order to better understand the development of cancer, researchers will study the changes in the HPV16 genome over a period of time in certain individuals. They will also study the mechanism of action of E7 on cancer risk in order to help develop therapeutic drugs for this protein. In addition, they will determine if their findings extend to other high-risk HPV types.
Researchers say their goal is to use existing findings to prevent or treat cervical cancer. Although this result does not change the HPV screening or vaccine, it may be important to understand which HPV infection poses the greatest cancer risk. Patients diagnosed with HPV16 infection and lesions require careful further diagnostic evaluation. This work raises the future goals of therapeutic intervention, but it also requires a lot of work.
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