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Background
Papillomaviruses are viruses that cause squamous epithelial and fibroepithelial tumors in their specific host species. In humans, human papillomaviruses (HPVs) can lead to both benign and malignant cell overgrowth, resulting in a wide range of clinical manifestations from genital warts to cervical cancer. HPV infection is the most common sexually transmitted disease, and over 4 types of HPV have been identified to infect the genital tract. Genital HPVs can be categorized as "low-risk" types such as HPV 6 and 11, or "high-risk" types including HPV 16, 18, 31, 33, 35, 39, 45, 52, and 58. The high-risk types are responsible for more than 95% of HPV-induced cervical cancer cases. Preventing cervical cancer through vaccination is considered the most effective approach. Prophylactic HPV vaccines have shown efficacy in clinical trials against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts. However, these vaccines only target a few specific HPV types. The vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. VLPs consist of 36 copies of L1 protein arranged into 72 pentamers or capsomeres, forming structures that are immunologically similar to native virions. The VLPs induce a type-specific immune response, with minor cross-neutralization observed mainly between closely related HPV types. Structural analysis has revealed the presence of hypervariable loops on the outer surface of the capsid. Most HPV-neutralizing monoclonal antibodies identified to date are type-specific and recognize conformational epitopes within these surface-exposed hypervariable loops of the L1 protein. This specificity is due to the unique characteristics of each HPV type.
Figure 1. Vaccination against HPV infection using genotype-specific HPV L1 VLPs. (Source: Berzofsky, J. A. et al., 2004)
Anti-HPV 39 L1 monoclonal antibodies are specialized antibodies designed to specifically recognize and bind to the L1 protein of HPV 39. They have significant applications in HPV research, diagnostics, and potentially targeted therapies. These antibodies help researchers understand the biology of HPV and provide potential avenues for developing novel interventions against HPV 39 infection and related diseases.
Alternative Names
Anti-HPV 39 L1 monoclonal antibody Anti-Human Papillomavirus 39 L1 monoclonal antibody Anti-Human papillomavirus type 39 L1 monoclonal antibody Anti-HPV39 major capsid protein L1 monoclonal antibody Anti-Human Papilloma Virus Type 39 major capsid protein L1 monoclonal antibody
References
1. Berzofsky J A, et al. Progress on new vaccine strategies against chronic viral infections. The Journal of Clinical Investigation. 2004, 114(4): 450-462.
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Infection with HPV (human papillomavirus) 16 is the cause of 50% or more of cervical cancers in women. HPV16 infection, however, is very common in young sexually active women, but the majority mount an effective immune response and clear infection. Approx. 10% of individuals develop a persistent infection, and it is this cohort who are at risk of cancer progression, with the development of high-grade precursor lesions and eventually invasive carcinoma. Effective evasion of innate immune recognition seems to be the hallmark of HPV infections, since the infectious cycle is one in which viral replication and release is not associated with inflammation. Furthermore, HPV infections disrupt cytokine expression and signalling with the E6 and E7 oncoproteins particularly targeting the type I IFN (interferon) pathway. High doses of IFN can overcome the HPV-mediated abrogation of signalling, and this may be the basis for the therapeutic effects on HPV infections of immune-response modulators such as the imidazoquinolones that induce high levels of type I IFNs by activation of TLR (Toll-like receptor) 7. Using the unique W12 model of cervical carcinogenesis, some of these IFN-related interactions and their relevance in the selection of cells with integrated viral DNA in cancer progression have been investigated. Our data show that episome loss associated with induction of antiviral response genes is a key event in the spontaneous selection of cervical keratinocytes containing integrated HPV16. Exogenous IFN-β treatment of W12 keratinocytes in which the majority of the population contain episomes results only in the rapid emergence of IFN-resistant cells, loss of episome-containing cells and a selection of cells containing integrated HPV16 in which the expression of the transcriptional repressor E2 is down-regulated, but in which E6 and E7 are up-regulated.
Genital human papillomavirus (HPV) infection with both low- and high-risk types is common, but most infections resolve as a result of a cell-mediated immune response. Failure to induce an effective immune response is related to inefficient activation of innate immunity and ineffective priming of the adaptive immune response; this defective immune response facilitates viral persistence, a key feature of high-risk HPV infection. This milieu becomes operationally HPV antigen tolerant, and the host's defenses become irrevocably compromised. HPV antigen-specific effector cells are poorly recruited to the infected focus and their activity is downregulated; neoplastic HPV containing cervical keratinocytes expressing high levels of E6 and E7 oncoproteins are not killed in this immunosuppressive, tolerant milieu, and progression to high-grade disease and cancer can result. Highly efficacious prophylactic HPV L1 virus-like particle (VLP) vaccines circumvent viral epithelial evasion strategies since they are delivered by intramuscular injection. The stromal dendritic cells of the muscle that encounter the highly immunogenic repeat structure of the VLP then migrate with their cargo to the lymph node, initiating an immune cascade that results in a robust T-cell dependent B-cell response, which generates high levels of L1-specific serum neutralizing antibodies and immune memory.
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Figure 1. Vaccination against HPV infection using genotype-specific HPV L1 VLPs.
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