Anti-HPV 52 L1 monoclonal antibody (set)

Human papillomavirus (HPV) has been linked to 5% of all cancers, including cervical, penile, vulvar, vaginal, anal and oropharyngeal cancers, with more than 95% of cervical cancers linked to HPV. The burden of cervical disease is unevenly distributed, with higher incidence and mortality rates of cervical cancer cases in low- and middle-income countries due to inadequate cervical cancer screening and treatment programs. HPV viruses consist of 72 pentameric capsids containing a circular double-stranded DNA genome that encodes a regulatory region, two structural proteins (L1 and L2) and early proteins (E1-E7). Early proteins are involved in viral replication and high-risk HPV carcinogenesis, with L1 being the major capsid protein and L2 being a secondary structural protein that forms the capsid. L1 was also selected as the basis for the design of the current human HPV vaccine because of its ability to self-assemble into virus-like particles (VLPs). HPVs are classified into subtypes based on differences in L1 gene sequences, with less than 45% homology of L1 sequences across subfamilies and less than 60% homology across genera. HPVs of the same genus can be further categorized into different types or species.

Figure 1. Proportion of HPV-related cervical cancers (squamous and glandular lesions) attributed to different HPV genotypes
(Source: Mariani L, et al. 2017)

The HPV L1 protein assembles into VLPs to induce HPV-type-specific antibodies, which form the basis of all commercial HPV vaccines. The researchers first demonstrated that VLPs prevent infection in an animal model by using a baculovirus expression system to produce the canine oral papillomavirus (COPV) L1 gene and injecting it into beagles, which demonstrated that the vaccinated animals were resistant to COPV. In addition, passive infusion of serum immunoglobulin also protected against infection, confirming that this protection was antibody-mediated. The remaining models of papillomavirus attack further confirmed that vaccines designed based on L1 VLPs are effective prophylactic vaccines, and these results, along with the evidence that HPV L1 can be assembled into VLPs, provide proof-of-concept for HPV vaccine development.

There are a number of HPVs that can cause cancer in humans and are categorized as Group 1, with HPV16 predominating. Other studies have also shown that HPV types 18, 31, 33, 52, 58 and 59 cause cervical cancer. In the uterine cervix, the contribution of non-HPV16/HPV18 genotypes to HPV-associated tumorigenesis is about 30%. HPV vaccination induces high levels of HPV type-specific antibodies, much higher titers than those induced by natural infection. Commercial HPV vaccines were initially developed around HPV16 and HPV18 as bivalent vaccines against HPV16 and HPV18 (2vHPV), and later as tetravalent vaccines against HPV6, HPV11, HPV16, and HPV18 (4vHPV), which prevented high-grade intraepithelial lesions in the female genital region (cervix, vagina, and vulva) more than 90%. These vaccines also produced indirect immune cross-reactivity, but elicited immune responses of lower intensity and duration than the targeted vaccine genotypes, and had poor clinical efficacy, so the subsequent nine-valent vaccine increased the number of targeted HPV types to include five high-risk genotypes (HPV31, HPV33, HPV45, HPV52, and HPV58).

Anti-Human papillomavirus 52 L1 monoclonal antibody
Anti-Human papillomavirus type 52 L1 monoclonal antibody