Recombinant full-length HPV oncoprotein E7, type 18.
Conjugate
Unconjugated
Product Background
Antigen Description
Infection with specific types of HPV has been associated with an increased risk of developing cervical neoplasia. HPV types 6 and 11 have been associated with relatively benign diseases such as genital warts but types 16 and 18 are strongly associated with cervical, vaginal, and vulvar malignancies. E7-driven degradation of pRb may be involved in cervical tumorigenesis in humans.
Citations
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Background
Human papillomavirus (HPV) first showed up in human warts and was shown, post 1970, directly to be a risk factor for cervical cancer. HPV is a tissue- or epithelial-, non-enveloped, double-stranded DNA virus. We now recognise over 200 HPV subtypes for humans – all of them structurally, functionally and pathologically high- or low-risk. – High risk HPV starts cervical cancer, the most common form of the disease. Among the strains that are most likely to be a risk are HPV16 and HPV18.
HPV travels into the cervical epithelium via punctured cervical epithelial cells, and then lands on the basal layer cells of the cervical epithelium where it proliferates and grows, slowly spreading to the surface layer of the cervical epithelium. Integrated integration of risk HPV DNA into the host genome occurs in most cervical cancer patients. There are three gene regions in HPV, including a long control region, an early gene region and a late gene region. HPV E6/E7 genes are oncogenes and HPV E6/E7 mRNA is required for cervical cancer development and spread. HPV is still generating E6/E7 mRNA, by hacking host DNA and producing E6/E7 proteins. Since the E2 gene is destroyed and the E6/E7 oncogenes are overexpressed, carcinogenesis follows. E6 and E7 attach to tumour suppressor proteins p53 and retinoblastoma protein (Rb), knocking out the tumor suppressor p53 and breaking down Rb, which changes cell cycle and DNA repair. This makes cells divide faster and leads to apoptosis, which causes the immortalisation of cells, leading to precancerous lesions and cervical cancer.
Figure 1. The joint action of HPV E6 and E7 oncoproteins is required for HPV-induced malignancy (Source: Tomaić V. 2016)
Cytological test and HPV-DNA testing are the two most popular cervical cancer tests. But cytological testing is highly false-negative, and HPV-DNA testing is positive screening for the majority of cases but fails to detect precancerous changes, or even the risk of cervical cancer. An mRNA test of HPV E6/E7, which targets the E6/E7 gene, not only indicates HPV infection and expression of the HPV E6/E7 oncogenes, it also can help determine the degree of activity of cervical lesions. It is a better predictor of potential for high-grade lesions or cancer.
1. Tomaić V. Functional Roles of E6 and E7 Oncoproteins in HPV-Induced Malignancies at Diverse Anatomical Sites. Cancers (Basel). 2016 Oct 19;8(10):95.
2. Yu L, et al. HPV16 and HPV18 Genome Structure, Expression, and Post-Transcriptional Regulation. Int J Mol Sci. 2022 Apr 29;23(9):4943.
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Publication 
Figure 1. The joint action of HPV E6 and E7 oncoproteins is required for HPV-induced malignancy
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