Abstract
To investigate the distribution of Human papillomavirus (HPV)-31 A, B and C variants as well as the common amino acid polymorphisms in Chinese women, all 14 HPV-31 positive cervical exfoliated cell specimens identified from a descriptive study including ∼2700 women from Northern China were analyzed. HPV-31 positive specimens were identified by Mass Spectrometry and the fragments of partial Long Control Region, E6 and E7 were amplified and directly sequenced or cloned into vector and then sequenced to confirm the variant information. HPV-31 prevalence in Northern Chinese female population was 0.52%. Six different sequences represented all 14 isolates, and these isolates were subsequently classified into variant lineage A (9), B (0) and C (5) by phylogenetic analysis. Five common amino acid polymorphism sites (2 in E6 and 3 in E7) and a novel non-synonymous mutation were detected in the current study. Our investigation suggested that HPV-31 was much less detected in Chinese women population than that in western countries. A and C variants were commonly detected while B variants were rarely detected in this population.
Highlights
Human papillomavirus (HPV) is a family of double strand DNA viruses
Five novel isolates were identified from 14 HPV-31 positive specimens
We found that the prevalence of HPV31 in northern Chinese women was 0.52% (95%CI: 0.28%– 0.87%)
Summary
Human papillomavirus (HPV) is a family of double strand DNA viruses. The classification of HPV is based on the conserved L1 sequence coding for the major capsid protein [1]. HPV can be classified as types, subtypes and variants when the differences between their L1 sequences are more than 10%, 10%–2% and less than 2%, respectively [1]. According to the carcinogenicity in cervical cancer, HPVs are classified as high risk and low risk types [3]. Persistent infection of high risk types has been proven to be a necessary cause of cervical cancer and risk factor of some other epithelial-derived carcinomas, such as ano-genital and oropharyngeal cancer etc. It has been reported that the potentiality of carcinogenesis is different among HPV variants. Nonsynonymous mutations in the E6, E7 oncogenes in HPV genome may alter the biological or immunogenic properties of the encoded protein, causing discrepancies in carcinogenicity of variants [6]
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