Persistence of human papillomavirus 16, 18 and 52 variants in Inuit women from Northern Quebec, Canada

Abstract

Intratypic DNA polymorphism has been described for human papillomavirus (HPV) types infecting Inuit women in Nunavik, Quebec, a high-risk population for HPV infection and cervical cancer, but there is no previous research on the association between HPV polymorphism and infection persistence in Inuit women. Polymorphism of HPV types 16, 18 and 52 was described in a subset of 64 participants with multiple clinic visits within a cohort of 677 Nunavik Inuit women aged 15-69 recruited in 2002-2010 with testing results. Logistic regression and Cox proportional hazards models were used to assess the association between HPV variants and infection persistence and clearance. Infections with HPV16 lineage A3 variants cleared 3.13 times faster (95% CI: 1.10-8.97) than those with lineage A1 variants. HPV52 lineage C variants cleared slower than lineage A variants (HR = 0.28, 95% CI: 0.08-0.98). HPV polymorphism may be associated with viral persistence for certain HPV types in this population.

Evaluating the Efficacy of Pervistop®, a New Combination Based on EGCG, Folic Acid, Vitamin B12 and Hyaluronic Acid on Patients with Human Papilloma Virus (HPV) Persistent Infections and Cervical Lesions: A Pilot Study

“…The persistence phenomenon is important as it is a risk factor in the integration of viral DNA in the host genome [ 6 ]. The integration of the genome is the real risk factor for the occurrence of transformation of the epithelium: the virus strains with the greatest oncogenic risk (HR-HPV), in particular HPV-16 and -18, are those that have the greatest persistence [ 7 ]. As a viruses persistence mainly depends on viral DNA integration into the cellular genome, and on the properties of the different viral strains to evade the immune response of the host, HPV-16 and -18 are the strains that expose the patients to a higher transforming risk.…”

The possible impact of novel mutations in human papillomavirus 52 on the infection characteristics

“…The prevalence of variation T350G (L83V) in HPV16 E6 in the population of persistent infection was found, albeit controversial, as the conflicting result was also retrieved [14][15][16][17]. Similarly, HPV52 lineage C variants displayed a slower clearance than lineage A [18], and non-prototype long control region (LCR) was found to be correlated with HPV52 persistence [19]. However, no specific variation in HPV52 was reported to shape the infection pattern.…”