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Introduction
Human papillomavirus (HPV) is a DNA virus from the papillomavirus family that is capable of infecting humans. Like all papillomaviruses, HPVs establish productive infections only in keratinocytes of the skin or mucous membranes. L1 is a major capsid protein of human papilloma virus. Infection with specific types of HPV has been associated with an increased risk of developing cervical neoplasia. Does not bind DNA.
Keywords
HPV 59 L1; HPV; HPV 59 VLP; HPV 59
Citations
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Background
Human papillomaviruses (HPV), known as DNA viruses from the Papillomaviridae family, are the most common sexually transmitted viral infections in women under the age of 34. Persistent infection with different HPVs can lead to atypical cervical hyperplasia and epithelial abnormalities, with high-risk HPVs (including 16, 18, 31, and 59) having the potential to lead to the development of cervical cancer.
HPV 59 is a tumorigenic virus that is associated with HPV 18, which was originally cloned from a vulvar intraepithelial neoplasia. HPV 59 shares high homology with HPV 18 (71%), 45 (70%), and 39 (69%) by comparative analysis of the HPV 59 genome with other HPVs. These HPV types have been linked to a high risk of cervical dysplasia. The L1 major capsid protein, which shares 73-75% homology with HPV types 18, 39 and 45, is encoded by the most conservative open reading frame. There are few studies in the literature on the pathogenicity of HPV 59. Some studies suggest that HPV 59 may be less carcinogenic, with a prevalence of only 1% to 3%, and some investigators have found that HPV 59 may cause precancerous and cancerous lesions in the absence of HPV 16 and HPV 18. There may be important clinical implications of these differences in HPV gene distribution.
In scientific studies, researchers have already established an HPV-immortalized cell line using HPV 59, which was cultured in mouse thymus xenografts with highly pleomorphic cells containing many abnormally shaped nuclei and mitotic elephants, and verified the complete viral growth cycle, including the production of infectious virus, through a series of experiments. Creative Diagnostics can provide recombinant HPV 59 L1 VLP and other related products that can better assist you in your scientific research.
Figure 1. Diagram representing the HPV 59 transcript (Source: Lehr EE, et al. 2003)
Alternative Names
Human papillomavirus type 59 L1 protein Human papillomavirus 59 L1 protein HPV 59 L1
References
1. Lehr EE, et al. Human papillomavirus type 59 immortalized keratinocytes express late viral proteins and infectious virus after calcium stimulation. Virology. 2003 Sep 30;314(2):562-71.
2. Ye F, et al. High prevalence of HPV59 in cytologically abnormal cervical samples. Exp Mol Pathol. 2015 Dec;99(3):611-6.
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References
Evidence for Missing Positive Results for Human Papilloma Virus 45 (HPV-45) and HPV-59 with the SPF10-DEIA-LiPA25 (Version 1) Platform Compared to Type-Specific Real-Time Quantitative PCR Assays and Impact on Vaccine Effectiveness Estimates
J Clin Microbiol
Authors: van Eer K, Leussink S, Severs TT, van Marm-Wattimena N, Woestenberg PJ, Bogaards JA, King AJ.
Human papillomavirus (HPV) epidemiological and vaccine studies require highly sensitive HPV detection systems. The widely used broad-spectrum SPF10-DEIA-LiPA25 (SPF10 method) has reduced sensitivity toward HPV-45 and -59. Therefore, anogenital samples from the PASSYON study were retrospectively analyzed with type-specific (TS) HPV-45 and -59 real-time quantitative PCR (qPCR) assays. The SPF10 method missed 51.1% of HPV-45 and 76.1% of HPV-59 infections that were detected by the TS qPCR assays. The viral copy number (VCn) of SPF10-missed HPV-45 and -59 was significantly lower than SPF10-detected HPV-45 and -59 (P < 0.0001 for both HPV types). Sanger sequencing showed no phylogenetic distinction between SPF10-missed and SPF10-detected HPV-59 variants, but variants bearing the A6562G single-nucleotide polymorphism (SNP) in the SPF10 target region were more likely to be missed (P = 0.0392). HPV cooccurrence slightly influenced the detection probability of HPV-45 and -59 with the SPF10 method. Moreover, HPV-59 detection with the SPF10 method was hampered more in nonvaccinated women than vaccinated women, likely due to a stronger masking effect by increased HPV cooccurrence in the former group. Consequently, the SPF10 method led to a strong negative vaccine effectiveness (VE) of -84.6% against HPV-59, while the VE based on TS qPCR was 3.1%. For HPV-45, the relative increase in detection in nonvaccinated women compared vaccinated women was more similar, resulting in comparable VE estimates. In conclusion, this study shows that HPV-45 and -59 detection with the SPF10 method is dependent on factors including VCn, HPV cooccurrence, and vaccination, thereby showing that knowledge of the limitations of the HPV detection method used is of great importance
Genetic diversity of human papillomavirus (HPV) as specified by the detection method, gender, and year of sampling: a retrospective cross-sectional study
Purpose: This study assesses HPV prevalence and genotype distribution in Lebanon, and identifies differentials in HPV infection, infection with multiple genotypes, and with high-risk genotypes, by sex, age, and year of data collection.
Methods: Study participants comprised 1042 female and 160 male participants between 2006 and 2018. HPV genotyping was done by PCR and hybridization (2006-2013) or real-time PCR (2013 onwards). Diversity of HPV genotypes across gender, age groups, and years of data collection was tested by applying Shannon Diversity Index.
Results: The overall HPV prevalence was 44.8% among study participants, and threefold higher in women than men. Single HPV infection was seen in two-third of HPV-positive participants. Women were less likely to be infected with multiple HPV strains, but more likely to be infected with high-risk or mixed-risk HPV genotypes. HPV-16 (11.0%, 9.8%) and HPV-53 (8.5%, 4.9%) were the most prevalent high-risk HPV genotypes in women and men, respectively, while HPV-18 prevalence was 4.9% in men and 3.1% in women, while HPV-59 prevalence was 6.6% in men and 2.1% in women. Samples collected post-2011 from women showed twice higher odds of HPV infection than those collected earlier and were threefold more likely to be infected with multiple HPV strains, and twice more likely to be infected with high-risk genotypes compared to those tested earlier. Women scored higher on Shannon index indicating high diversity in HPV types and frequency, with trend of increased diversity over time. While the odds of HPV infection remained associated with sex and temporal trend in multivariable analysis, odds of having high-risk genotypes was mainly associated with infection with multiple HPV strains.
Conclusion: Our study showed high diversity in HPV genotypes and an increasing trend of infection with multiple and high-risk genotypes in recent years. Findings underscore the need for effective screening/surveillance and HPV vaccination programs
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Figure 1. Diagram representing the HPV 59 transcript
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