IC50(μg/ml) for Neut: 1B1-97; 3A2-0.00030; 3A4-1.46; 4H1-0.76; 4H5-1.31; 7H8-0.0025
Target
Alternative Names
HPV; L1; major capsid L1 protein; HPV-18; HPV-18 capsid; HPV18 capsid protein; HPV18 L1; HPV18 major capsid protein L1; Human papillomavirus type 18 L1; Human papillomavirus type 118 major capsid protein L1; Major capsid protein; Major capsid protein L1; Human papillomavirus
Citations
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Background
HPV is a small, non-enveloped DNA virus. More than 100 types of HPV have been discovered so far, divided into high-risk and low-risk types. Studies have found that the life cycle of HPV is closely related to the biology of keratinocytes. Keratinocytes are involved in the formation of the outer layer of the skin (epidermis) and the surface of other stratified squamous epithelium. Therefore, HPV infection occurs mostly in areas rich in keratinocytes such as the genitals, oral cavity, and esophagus. Later stages of the viral life cycle, when new virions are assembled, occur only in keratinocytes that undergo terminal differentiation steps, ultimately leading to desquamation (the shedding of dead keratinocytes into the environment). Molecular epidemiological surveys have shown that certain types of persistent infection are closely related to the occurrence of cervical cancer, and the detection rate of HPV DNA in all cervical cancer specimens is as high as 80%. HPV18 is the second most common high-risk HPV in cervical cancer patients in most parts of the world, after HPV16, but HPV18 has a stronger malignant transformation ability than HPV16. Human papillomavirus (HPV) belongs to the Papillomaviridae family. The genome is about 8000 base pairs (bp) long and is divided into 3 functional regions. That is, the early transcribed region (E region), the late transcribed region (L region) and the non-transcribed region (LCR). Previous studies have made it clear that HPV is the culprit of cervical cancer. However, not all HPV types cause cervical cancer. Among samples of cervical cancer patients worldwide, HPV16 infection rate is the highest, followed by HPV18.
Figure 1. Structural representation of HPV and the L1 protein used as antigen in current vaccines.(Source: Kombe Kombe AJ, et al., 2021)
The outer surface of HPV particles has a nodular structure. The diameter of HPV virus particles is 55 ~ 60nm. The nucleocapsid is icosahedron symmetrical and consists of 72 pentamers of the major capsid protein L1 and the minor capsid protein L2. The N- and C-termini of L1 are arranged as extended "invasion arms" that form the floor between the capsomer knobs. The C terminus of L1 is particularly complex. Each C-terminal intrusion arm wraps the canyon-facing surface of the invading capsomer to a point near the outer apex of the knob. At this high apical point, an inter-L1 disulfide bond forms between adjacent capsomeres. L1 is translated from RNA, and its transcription is thought to initiate from the common upstream regulatory region (URR) of early and late genes. In order to reach the late region containing the L1 gene, the transcription machinery must pass through the genes in the early region. Post-transcription of L1 mRNA requires the removal of early gene sequences present on the pre-mRNA through splicing. HPV18 L1 refers to the capsid protein L1 of the HPV18 type. It is an approximately 55 kD protein. A large number of studies have confirmed that HPV L1 protein is the main target protein of HPV vaccines. The HPV L1 protein expressed in a variety of expression systems can form virus-like particles (VLP) that are similar in morphological structure to natural virus particles without the assistance of L2 protein. The recombinant HPV L1-VLP vaccine has been successfully marketed and used to prevent HPV infection and the resulting diseases such as cervical cancer and genital warts. It has been fully proven that L1-VLP has the same antigenicity and immunogenicity as wild viruses of the same type. Judging from the tertiary structure of VLP, its antigenic determinants are distributed on the surface of the pentamer, the basic structural unit of VLP. This shows that the antigenicity and immunogenicity of HPV L1-VLP originate from or depend on the pentamer composed of L1. Therefore, the recombinant L1 protein pentamer has complete antigenic epitopes like VLP- and can also be used as an antigen to prepare vaccines.
Alternative Names
HPV-18 Shell Protein HPV-18 Capsid Protein HPV-18 Coat Protein HPV-18 Major Capsid Protein HPV-18 Structural Protein HPV-18 Viral Capsid Protein L1 HPV-18 Outer Capsid Protein HPV-18 Shell Component L1 HPV-18 Capsomer Protein L1 HPV-18 Surface Antigen L1
References
1. Kombe Kombe AJ, et al., Epidemiology and Burden of Human Papillomavirus and Related Diseases, Molecular Pathogenesis, and Vaccine Evaluation. Front Public Health. 2021, 8:552028.
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References
Genetic Diversity in the Major Capsid L1 Protein of HPV-16 and HPV-18 in the Netherlands
PLoS One
Authors: King AJ, Sonsma JA, Vriend HJ, van der Sande MA, Feltkamp MC, Boot HJ, Koopmans MP
Objectives: Intratypic molecular variants of human papillomavirus (HPV) type-16 and -18 exist. In the Netherlands, a bivalent vaccine, composed of recombinant L1 proteins from HPV-16 and -18, is used to prevent cervical cancer since 2009. Long-term vaccination could lead to changes in HPV-16 and -18 virus population, thereby hampering vaccination strategies. We determined the genetic diversity of the L1 gene in HPV-16 and -18 viral strains circulating in the Netherlands at the start of vaccination in order to understand the baseline genetic diversity in the Dutch population.
Methods: DNA sequences of the L1 gene were determined in HPV-16 (n = 241) and HPV-18 (n = 108) positive anogenital samples collected in 2009 and 2011 among Dutch 16- to 24-year old female and male attendees of the sexually transmitted infection (STI) clinics. Phylogenetic analysis was performed and sequences were compared to reference sequences HPV-16 (AF536179) and HPV-18 (X05015) using BioNumerics 7.1.
Results: For HPV-16, ninety-five single nucleotide polymorphism (SNPs) were identified, twenty-seven (28%) were non-synonymous variations. For HPV-18, seventy-one SNPs were identified, twenty-nine (41%) were non-synonymous. The majority of the non-silent variations were located in sequences encoding alpha helix, beta sheet or surface loops, in particular in the immunodominant FG loop, and may influence the protein secondary structure and immune recognition.
Conclusions: This study provides unique pre-vaccination/baseline data on the genetic L1 diversity of HPV-16 and -18 viruses circulating in the Netherlands among adolescents and young adults.
Efficacy of the bivalent HPV vaccine against HPV 16/18-associated precancer: long-term follow-up results from the Costa Rica Vaccine Trial
Background: Oncogenic human papillomavirus (HPV) infections cause most cases of cervical cancer. Here, we report long-term follow-up results for the Costa Rica Vaccine Trial (publicly funded and initiated before licensure of the HPV vaccines), with the aim of assessing the efficacy of the bivalent HPV vaccine for preventing HPV 16/18-associated cervical intraepithelial neoplasia grade 2 or worse (CIN2+).
Methods: Women aged 18-25 years were enrolled in a randomised, double-blind, controlled trial in Costa Rica, between June 28, 2004, and Dec 21, 2005, designed to assess the efficacy of a bivalent vaccine for the prevention of infection with HPV 16/18 and associated precancerous lesions at the cervix. Participants were randomly assigned (1:1) to receive an HPV 16/18 AS04-adjuvanted vaccine or control hepatitis A vaccine. Vaccines were administered intramuscularly in three 0·5 mL doses at 0, 1, and 6 months and participants were followed up annually for 4 years. After the blinded phase, women in the HPV vaccine group were invited to enrol in the long-term follow-up study, which extended follow-up for 7 additional years. The control group received HPV vaccine and was replaced with a new unvaccinated control group. Women were followed up every 2 years until year 11. Investigators and patients were aware of treatment allocation for the follow-up phase. At each visit, clinicians collected cervical cells from sexually active women for cytology and HPV testing. Women with abnormal cytology were referred to colposcopy, biopsy, and treatment as needed. Women with negative results at the last screening visit (year 11) exited the long-term follow-up study. The analytical cohort for vaccine efficacy included women who were HPV 16/18 DNA-negative at vaccination. The primary outcome of this analysis was defined as histopathologically confirmed CIN2+ or cervical intraepithelial neoplasia grade 3 or worse associated with HPV 16/18 cervical infection detected at colposcopy referral. We calculated vaccine efficacy by year and cumulatively. This long-term follow-up study is registered with ClinicalTrials.gov, NCT00867464.
Findings: 7466 women were enrolled in the Costa Rica Vaccine Trial; 3727 received the HPV vaccine and 3739 received the control vaccine. Between March 30, 2009, and July 5, 2012, 2635 women in the HPV vaccine group and 2836 women in the new unvaccinated control group were enrolled in the long-term follow-up study. 2635 women in the HPV vaccine group and 2677 women in the control group were included in the analysis cohort for years 0-4, and 2073 women from the HPV vaccine group and 2530 women from the new unvaccinated control group were included in the analysis cohort for years 7-11. Median follow-up time for the HPV group was 11·1 years (IQR 9·1-11·7), 4·6 years (4·3-5·3) for the original control group, and 6·2 years (5·5-6·9) for the new unvaccinated control group. At year 11, vaccine efficacy against incident HPV 16/18-associated CIN2+ was 100% (95% CI 89·2-100·0); 34 (1·5%) of 2233 unvaccinated women had a CIN2+ outcome compared with none of 1913 women in the HPV group. Cumulative vaccine efficacy against HPV 16/18-associated CIN2+ over the 11-year period was 97·4% (95% CI 88·0-99·6). Similar protection was observed against HPV 16/18-associated CIN3-specifically at year 11, vaccine efficacy was 100% (95% CI 78·8-100·0) and cumulative vaccine efficacy was 94·9% (73·7-99·4). During the long-term follow-up, no serious adverse events occurred that were deemed related to the HPV vaccine. The most common grade 3 or worse serious adverse events were pregnancy, puerperium, and perinatal conditions (in 255 [10%] of 2530 women in the unvaccinated control group and 201 [10%] of 2073 women in the HPV vaccine group). Four women in the unvaccinated control group and three in the HPV vaccine group died; no deaths were deemed to be related to the HPV vaccine.
Interpretation: The bivalent HPV vaccine has high efficacy against HPV 16/18-associated precancer for more than a decade after initial vaccination, supporting the notion that invasive cervical cancer is preventable.
COA
Publication 
Figure 1. Structural representation of HPV and the L1 protein used as antigen in current vaccines.(Source: Kombe Kombe AJ, et al., 2021)
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