Background
Human papillomavirus (HPV) is a group of highly contagious double-stranded DNA viruses that spread largely through cutaneous and sexual contact. HPV is classed as high-risk or low-risk based on its pathogenicity and infection site. Human papillomavirus type 6 (HPV 6) is a low-risk HPV that was initially isolated from genital warts (GWs), also known as anal-genital warts or condylomata acuminata, in 1981. The viral particles are around 55 nanometers in diameter and covered in a protein shell. The L1 protein is the primary outer shell protein of HPV 6 virions, responsible for the viral shell's production and stability. L1 protein is also thought to play an important role in viral infection, mediating the virus's entry into host cells as well as its assembly and release throughout the viral life cycle. The HPV life cycle begins when the virus enters host cells via wounds or micro-abrasions in the basal layer of the epithelium. The L1 protein binds to laminin in the basement membrane first, then undergoes a sequence of conformational changes that allow it to bind to epithelial cell surfaces. Ultimately, the virus is ingested by endocytosis. Once inside, the viral DNA is released into the nucleus and leverages the host cell's replication and transcription machinery to generate many viral genomes and structural proteins, resulting in the formation of new viral particles. During epithelial cell differentiation, these particles are discharged into the environment, bringing the viral life cycle to an end.
Figure 1. Schematic of the HPV Life Cycle (Source: Mlynarczyk-Bonikowska B, et al., 2024)
When infected, HPV 6 often produces skin or mucous membrane lesions, with genital warts being the most prevalent manifestation, which appear as tiny, soft, flesh-colored, or grayish-white growths in the genital or surrounding areas. Some infected people may have mild or severe itching in the genital area, while others may experience odd odors or irregular urine symptoms linked with genital warts. During the initial stages of infection, the host's immune system works to recognize and eliminate the virus. Many infected people are asymptomatic and may be unaware they are infected, yet they can still transmit the virus to others. In some circumstances, particularly when the immune system is impaired, HPV 6 infection can result in persistent lesions. As a result, protecting oneself during sexual activity and getting frequent screenings are critical for avoiding and managing HPV infection. Furthermore, HPV 6 infection is linked to more serious disease states, such as cervical and genital tract malignancies, however, this is uncommon.
Currently, HPV 6 and its L1 protein have significant potential in vaccine and therapeutic research. As the main capsid protein of HPV 6, L1 can self-assemble into virus-like particles (VLPs) used in vaccine development. HPV vaccines (such as Gardasil and Cervarix) containing L1 protein VLPs effectively stimulate the immune system to produce protective antibodies, thereby preventing HPV infection and related diseases. Moreover, researchers are exploring the use of L1 protein as part of therapeutic strategies, attempting to leverage its role as a component of vaccines to treat HPV-related diseases, particularly in the context of high-risk HPV infections and cancer research.
Alternative Names
Mouse anti-HPV6 L1 mAb, Clone 2642
Mouse Monoclonal Antibody against HPV6 L1, Clone 2642
Anti-HPV6 L1 mAb, Clone 2642
References
- 1. Mlynarczyk-Bonikowska B, et al. HPV Infections—Classification, Pathogenesis, and Potential New Therapies. International Journal of Molecular Sciences. 2024; 25(14):7616.
References
Occurrence of human papillomavirus (HPV) type replacement by sexual risk-taking behaviour group: Post-hoc analysis of a community randomized clinical trial up to 9 years after vaccination (IV)
INTERNATIONAL JOURNAL OF CANCER
Authors: Gray, Penelope; Luostarinen, Tapio; Vanska, Simopekka; Eriksson, Tiina; Lagheden, Camilla; Man, Irene; Palmroth, Johanna; Pimenoff, Ville N.; Soderlund-Strand, Anna; Dillner, Joakim; Lehtinen, Matti
Abstract
Oncogenic non-vaccine human papillomavirus (HPV) types may conceivably fill the vacated ecological niche of the vaccine types. The likelihood of this may differ by the risk of acquiring HPV infections. We examined occurrence of HPV types among vaccinated and unvaccinated subgroups of 1992-1994 birth cohorts with differing acquisition risks up to 9 years post-implementation of HPV vaccination in 33 Finnish communities randomized to: Arm A (gender-neutral HPV16/18 vaccination), Arm B (girls-only HPV16/18 vaccination and hepatitis B-virus (HBV) vaccination of boys), and Arm C (gender-neutral HBV vaccination). Out of 1992-1994 born resident boys (31,117) and girls (30,139), 8,618 boys and 15,615 girls were vaccinated, respectively, with 20-30% and 50% coverage in 2007-2009. In 2010-2013, 8,868 HPV16/18 and non-HPV vaccinated females, and in 2014-2016, 5,574 originally or later (2010-2013) HPV16/18 vaccinated females attended two cervical sampling visits, aged 18.5 and 22-years. The samples were typed for HPV6/11/16/18/31/33/35/39/45/51/52/56/58/59/66/68 using PCR followed by MALDI-TOF MS. HPV prevalence ratios (PR) between Arms A/B vs. C were calculated for Chlamydia trachomatis positives (core-group), and negatives (general population minus core group). At both visits the vaccine-protected HPV type PRs did not significantly differ between the core-group and non-core group. Among the vaccinated 18-year-olds, HPV51 occurrence was overall somewhat increased (PRcore = 1.4, PRnon-core. = 1.4) whereas the HPV52 occurrence was increased in the core-group only (PRcore = 2.5, PRnon-core = 0.8). Among the non-HPV vaccinated 18-year-olds, the HPV51/52 PRs were higher in the core-group (PRcore = 3.8/1.8, PRnon-core = 1.2/1.1). The 22-year-olds yielded no corresponding observations. Monitoring of the sexual risk-taking core-group may detect early tendencies for HPV type replacement.
Distribution of Vaccine-Type Human Papillomavirus Does Not Differ by Race or Ethnicity Among Unvaccinated Young Women
JOURNAL OF WOMENS HEALTH
Authors: Whittemore, Dana; Ding, Lili; Widdice, Lea E.; Brown, Darron A.; Bernstein, David I.; Franco, Eduardo L.; Kahn, Jessica A.
Abstract
Background: Previous studies have demonstrated racial and ethnic differences in the distribution of human papillomavirus (HPV) types among adult women with cervical precancers. The aim of this study was to determine whether the distribution of vaccine-targeted HPV types varies by race/ethnicity among unvaccinated young women. Materials and Methods: A secondary analysis was performed using data from four studies of sexually experienced, unvaccinated, 13-26-year-old women. Participants completed surveys and provided a cervicovaginal swab for HPV DNA testing. Multivariable logistic regression analyses were performed to examine whether race, ethnicity, and other factors were associated with type-specific HPV infection among the overall sample and among HPV-infected participants. Models controlled for age, HPV knowledge, sexual behaviors, substance use, and random study effect. Results: The mean age of participants (N=841) was 19.3 years; 64.4% were black and 8.9% Hispanic. Black women were more likely than white women to be positive for 1 HPV type (odds ratio [OR] 1.83, 95% CI 1.30-2.58) and Hispanic women were less likely than non-Hispanic women to be positive for 1 HPV type (OR 0.47, 95% CI 0.24-0.92). However, among all young women and HPV-infected women, neither race nor ethnicity was associated with positivity for HPV types targeted by the following vaccines: 2-valent (HPV16 and/or 18), 4-valent (HPV6, 11, 16, and/or 18), or 9-valent (HPV6, 11, 16, 18, 31, 33, 45, 52, and/or 58). Conclusion: The prevalence of HPV types targeted by the 2-valent, 4-valent, and 9-valent vaccines did not differ by race or ethnicity among all and among HPV-infected women in this sample.