2014
DOI: 10.1371/journal.pone.0100746
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Abstract: HPV16 accounts for 50–70% of cervical cancer cases worldwide. Characterization of HPV16 variants previously indicated that they differ in risks for viral persistence, progression to cervical precancer and malignant cancer. The aim of this study was to examine the association of severity of disease with HPV16 variants identified in specimens (n = 281) obtained from a Cervical Pathology and Colposcopy outpatient clinic in the University Hospital of Espírito Santo State, Southeastern Brazil, from April 2010 to No… Show more

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Cited by 76 publications
(74 citation statements)
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References 77 publications
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“…This result suggests that non-European HPV16 variants are more oncogenic than European variants, and is in agreement with the findings of previous studies [5,44,59,60] demonstrating that HPV16 non-European viral variants were significantly more likely than European variants to cause persistence and a CIN3+ evolution [8,14,16,61] inducing proliferation phenotype in an organotypic epithelial model [45 ,46], probably due to 1) modification of the immunogenic properties of the virus [46,62,63], 2) stimulation of cell migration and cell invasion [64] and 3) viral DNA integration into the host genome [45,46].…”
Section: Discussionsupporting
confidence: 93%
See 1 more Smart Citation
“…This result suggests that non-European HPV16 variants are more oncogenic than European variants, and is in agreement with the findings of previous studies [5,44,59,60] demonstrating that HPV16 non-European viral variants were significantly more likely than European variants to cause persistence and a CIN3+ evolution [8,14,16,61] inducing proliferation phenotype in an organotypic epithelial model [45 ,46], probably due to 1) modification of the immunogenic properties of the virus [46,62,63], 2) stimulation of cell migration and cell invasion [64] and 3) viral DNA integration into the host genome [45,46].…”
Section: Discussionsupporting
confidence: 93%
“…Additional factors are likely to increase the probability of this progression occurring. For example, the percentage of HPV16 DNA integration, as a marker for high-grade cervical lesions, was demonstrated in some studies [23], while the increased frequency of non-European HPV16 variants in invasive lesions was described by Tornesello et al [43], suggesting greater oncogenicity for the nonEuropean HPV16 variants [44][45][46].…”
Section: Discussionmentioning
confidence: 96%
“…Several investigations have been carried out on the prevalence and distribution of HPV in different regions of Brazil (Villa et al, 2000;Sichero et al, 2007;de Medeiros Fernandes et al, 2008;Baldez da Silva et al, 2009;Fernandes et al, 2009Fernandes et al, , 2010Castro et al, 2011;Oliveira-Silva et al, 2011;Freitas et al, 2014;Chagas et al, 2015;Gurgel et al, 2013Gurgel et al, , 2015. The results of these studies have shown divergent HR HPV genotype distribution, although most have pointed to HPV16 as the most frequent type (with the exception of the study developed by Chagas et al, 2015).…”
Section: Discussionmentioning
confidence: 99%
“…1) (12)(13)(14)(15)(16). In particular, lineage D is reported to be preferentially associated with an increased risk of developing CIN3 or worse (CIN3+) (17)(18)(19)(20).…”
Section: Genetic Diversity Of Hpv16mentioning
confidence: 99%
“…T350G is located in E6 and causes an amino acid change at residue 83 of the E6 protein, from leucine to valine (L83V) (28)(29)(30). However, the association has not been consistently observed in other studies (16,21), which compromises the implication of this particular SNP in cervical carcinogenesis.…”
mentioning
confidence: 99%