Recombinant HPV type 16 L1 Protein

Human papillomavirus is a non-enveloped epithelial cell DNA double-stranded circular virus with a genome length of about 8 kb, and all gene transcription templates are located on one DNA strand. Its genome is divided into three regions: the early region, which has an early open reading frame (ORF) and encodes early non-structural proteins (E1-E8). The E1-E5 genes encode proteins primarily involved in the replication and transcription of the viral genome. The bicistronic E6 and E7 genes are responsible for oncogenic transformation of host cells; the late region, which has late ORFs, encoding late capsid proteins (L1, L2); the long control region (LCR), which contains cis-responsive elements, it has the functions of oncogene expression regulation and virus assembly. Among cervical cancer cases caused by HPV infection, about 55% are caused by HPV16, about 15% are caused by HPV18, and the remainder are caused by other high-risk HPV types. Normally, high-risk HPV causes short-lived infections, but the immune system clears the virus and generally does not lead to cancer. If persistent HPV infection is not detected and cleared by the immune system, it may cause cancer.

Figure 1. HPV-16 genome organization.(Source: Lulia Muntean, et al., 2015)

HPV enters infected cells through the network structure of single-layer squamous epithelial cells, or enters the body through damaged cells. The capsid of HPV is composed of two proteins, L1 and L2. The binding of HPV to cell surface receptors mainly relies on L1. The L1 binding site is located on the cell receptor on the basement membrane or basal cell surface. Taking HPV16 as an example, heparin sulfate protein Polysaccharides (HSPGs) are the main receptors for initial binding. When the two combine, the conformation of cyclophilin B in the capsid changes, exposing the N-terminus of L2 to the virus surface and being degraded by furin, etc., thereby allowing L1 to Secondary receptor binding. Cell receptors may also change depending on the HPV type and the infected cell. The L1 protein binds to specific receptors on the surface of the infected cell membrane, allowing the HPV genome to enter the cell through the endocytosis mechanism of the cell membrane, and then the free genes enter the nucleus through the tubulin-mediated pathway. The virus enters the nucleus through nuclear pores or the ruptured nuclear membrane during mitosis. At this time, because the HPV genome is in a naked state, studies have shown that 72% of cervical cancer cell biopsy samples can detect HPV ring-shaped The DNA genome is integrated into the genome of the host cell. But regardless of integration or not, the virus has to start its early transcription. When the virus enters cells, it is first necessary to correctly regulate the early promoter of the virus to ensure the continued survival of HPV-infected cells. Therefore, the RNA encoding the virus's replication factor E1 and transcription factor E2 is the first to be detected. E1 binds to E2 and binds to the viral origin of replication, initiating the cell's replication machinery. This is the first stage of HPV genome replication and genome maintenance. The E2 protein binds to the LCR and links its genome to the host cell chromosome. When cells enter the terminal stage of differentiation, the expression of the E6 and E7 genes of the virus is up-regulated, and at the same time, the large expression of the late capsid protein L1 and L2 genes of the HPV virus is initiated. Thereafter, the HPV genome and capsid protein self-assemble into the form of the virus within the cell, which is released from the cells at the infection site and enters the next infection cycle.

HPV16 L1 Capsid Protein
HPV16 Major Capsid Protein
HPV16 L1 Structural Protein
HPV16 L1 Subunit
HPV16 L1 Antigen
HPV16 L1 Immunogen
HPV16 L1 VLP Vaccine Antigen