Mouse Anti-HPV16 L1 Monoclonal antibody, clone 2646

Most cervical cancers occur due to long-term persistent infection with oncogenic human papillomavirus (HPV). The HPV genome is a double-stranded circular DNA that can be divided into a long control region (LCR), an early region encoding the early genes E1-E7, and a late region encoding the late genes L1 and L2. HPV can also be categorized into genera based on sequence similarity of the L1 gene. In order to initiate viral infection, L1 capsid protein will bind to heparin sulfate proteoglycans (HSPGs) on epithelial cell surface or basement membrane, or interact with laminin-332 on extracellular matrix. After binding, the virus capsid undergoes conformational modification mediated by cyclophilin (CyP) B, and finally the smaller capsid protein L2 is exposed.

Figure 1. Human papillomavirus structure and genomic organization. a. HPV structure; b. genomic organization of the HPV genome
(Source: Oumeslakht L, et al. 2021)

The HPV16 L1 gene is located between nucleotides 5559 and 7154 and encodes the major coat protein L1. The gene encoding the minor coat protein L2 is located between nucleotides 4235 and 5656. The L1 protein has specific conformational epitopes and the ability to self-assemble into virus-like particles (VLPs), which, together with the fact that it contains a number of very conserved regions, has been used in the design and development of prophylactic vaccines against HPV. Such VLPs are structurally and immunologically similar to true viral particles, but have no viral DNA, making them safe and non-infectious.

HPV vaccines are highly immunogenic due to the structural characteristics of L1 VLPs, which produce long-lasting antigen-specific antibody-producing cells. HPV bivalent, quadrivalent and nine-valent vaccines have been approved for different types of HPV. The immune response induced by the vaccine produces L1-specific neutralizing antibody titers that are 10-100 times higher than those produced in response to natural infection, resulting in the prevention of viral infections and the development of premalignant dysplasia. Antibodies produced by intramuscular vaccination are transferred to the site of viral infection by two mechanisms, primarily by direct transfer of interstitial antibodies at the site of injury in the basal epithelial cell layer, thereby blocking viral infection, and secondarily IgG may cross the epithelial layer into mucosal secretions via the neonatal Fc receptor expressed in the cervix. However, the latter may play only a secondary vaccine-protective role because the concentration of L1-specific neutralizing antibodies in the cervical mucus of vaccinated women is 10-100 times lower than in serum.

Anti-human papillomavirus 16 L1 Monoclonal antibody
Anti-human papillomavirus type 16 L1 Monoclonal antibody