Standard curve of H. pylori q-PCR assay.

<p>Standard curve of H. pylori q-PCR assay.</p

Concordance between diagnostic tests.

<p>Concordance between diagnostic tests.</p

Comparison of average <i>H</i>. <i>pylori</i> DNA between different diagnostic tests.

<p>Comparison of average <i>H</i>. <i>pylori</i> DNA between different diagnostic tests.</p

Relationship between average <i>H</i>. <i>pylori</i> bacterial load and endoscopic findings, sex and age.

<p>Relationship between average <i>H</i>. <i>pylori</i> bacterial load and endoscopic findings, sex and age.</p

Nucleotide sequences of primers and probes.

<p>Nucleotide sequences of primers and probes.</p

Percentage of biopsies testing positive for <i>H</i>. <i>pylori</i>.

<p>Percentage of biopsies testing positive for <i>H</i>. <i>pylori</i>.</p

Distribution of vaccinal and non-vaccinal genotypes according to age.

*<p> <b>n:220.</b></p>**<p> <b>n:108.</b></p><p><b>LR:</b> Low risk <b>HR:</b> High risk <b>lHR:</b> likely High risk <b>NT:</b> Non-typed.</p

Detected genotype distribution according to age.

<p>Detected genotype distribution according to age.</p

HPV incidence in males per years of study.

<p>HPV incidence in males per years of study.</p

Prevalence of HPV 16 and HPV 18 Lineages in Galicia, Spain

<div><p>Genetic variants of human papillomavirus types 16 and 18 (HPV16/18) could differ in their cancer risk. We studied the prevalence and association with high-grade cervical lesions of different HPV16/18 variant lineages in a case-control study including 217 cases (cervical intraepithelial neoplasia grade 2 or grade 3 or worse: CIN2 or CIN3+) and 116 controls (no CIN2 or CIN3+ in two-year follow-up). HPV lineages were determined by sequencing the long control region (LCR) and the E6 gene. Phylogenetic analysis of HPV16 confirmed that isolates clustered into previously described lineages: A (260, 87.5%), B (4, 1.3%), C (8, 2.7%), and D (25, 8.4%). Lineage D/lineage A strains were, respectively, detected in 4/82 control patients, 19/126 CIN3+ cases (OR = 3.1, 95%CI: 1.0–12.9, p = 0.04), 6/1 glandular high-grade lesions (OR = 123, 95%CI: 9.7–5713.6, p<0.0001), and 4/5 invasive lesions (OR = 16.4, 95%CI: 2.2–113.7, p = 0.002). HPV18 clustered in lineages A (32, 88.9%) and B (4, 11.1%). Lineage B/lineage A strains were respectively detected in 1/23 control patients and 2/5 CIN3+ cases (OR = 9.2, 95%CI: 0.4–565.4, p = 0.12). In conclusion, lineages A of HPV16/18 were predominant in Spain. Lineage D of HPV16 was associated with increased risk for CIN3+, glandular high-grade lesions, and invasive lesions compared with lineage A. Lineage B of HPV18 may be associated with increased risk for CIN3+ compared with lineage A, but the association was not significant. Large well-designed studies are needed before the application of HPV lineage detection in clinical settings.</p></div