Background: Human papillomavirus (HPV) is a causal agent for approximately 5.3% of cancers worldwide and is the main cause of cervical cancer1. HPV16, designed "high-risk" causes over half of all cervical cancer and some HPV16 variants are more oncogenic than others2. Persistent high grade SIL squamous intraepithelial lesions (HSILs), represents the precursor lesion of cervical cancer3. It is still to be elucidated if included nucleotides vary across and within HPV types and lineages, or which of the single nucleotide polymorphisms (SNPs) determine oncogenicity2. Objective: To characterize the HPV 16 genome of a rapidly progressive, cervical lesion in a 39-year-old woman.
Methods: Cervical biopsies from one woman with different HPV 16 lesions at two distinct time diagnosis (LSIL and progressive HSIL, with seven months interval) were analyzed by PCR and complete genome sequencing.
Results: The most frequently observed variations were in E7, in L1, and in the LCR regions and novel variants were identified.
Conclusions: Our data suggest that specific SNPs are associated with increased risk for severe cervical lesion and neoplasic evolution. Molecular mechanisms involved in SNPs in HPV 16 and tumor initiation and progression require further investigation.
References:
1-Roden RB, Monie A, Wu TC. Opportunities to improve the prevention and treatment of cervical cancer.CurrMol Med. 2007 Aug;7(5):490-503.
2-Smith B, Chen Z, Reimers L,Doorslaer K,Schiffman M, DeSalle R,Herrero R, Yu K, Wacholder S, Wang T,D. Burk RD. Sequence Imputation of HPV16 Genomes for Genetic Association Studies.PLoS One. 2011; 6(6): e21375.
3-Burd.EMHuman Papillomavirus and Cervical Cancer.ClinMicrobiol Rev. 2003 Jan; 16(1): 1–17.