BackgroundHuman papillomavirus (HPV) variants differ in their biological and chemical properties, and therefore, may present differences in pathogenicity. Most authors classified variants based on the phylogenetic analysis of L1 region. Nevertheless, recombination in HPV samples is becoming a usual finding and thus, characterizing genetic variability in other regions should be essential.ObjectivesWe aimed to characterize the genetic variability of HPV 18 in 5 genomic regions: E6, E7, E4, L1 and the Upstream Regulatory Region (URR), working with both single infection and multiple HPV infection samples. Furthermore, we aimed to assess the prevalence of HPV 18 variants in our region and look for possible existence of recombination as well as analyze the relationship between these variants and the type of lesion.MethodsFrom 2007 to 2010, Clinical Microbiology and Infection Control Department analyzed 44 samples which were positive for HPV 18. Genetic variability was determined in PCR products and variants were assigned to European, Asian-amerindian or African lineage. Recombination and association of variants with different types of lesion was studied.ResultsGenetic analysis of the regions revealed a total of 56 nucleotide variations. European, African and Asian-amerindian variants were found in 25/44 (56.8%), 10/44 (22.7%) and 5/44 (11.4%) samples, respectively. We detected the presence of recombinant variants in 2/44 (4.5%) cases. Samples taken from high-grade squamous intraepithelial lesions (H-SIL) only presented variants with specific-african substitutions.ConclusionsMultiple HPV infection, non-european HPV variants prevalence and existence of recombination are considered risk factors for HPV persistence and progression of intraepithelial abnormalities, and therefore, should be taken into consideration in order to help to design and optimize diagnostics protocols as well as improve epidemiologic studies.Our study is one of the few studies in Spain which analyses the genetic variability of HPV18 and we showed the importance of characterizing more than one genomic region in order to detect recombination and classify HPV variants properly.

BackgroundThe aims of this study were to detect HPV E6/E7 mRNA expression in women with high-risk genotypes (HPV-16, -18, -31, -33 and -45) analysing its relationship with tissue pathology and 2) 2-year follow-up of E6/E7 mRNA tested group.MethodsOur samples were genotyped and classified by pathologists according to Bethesda system. After RNA extraction, E6/E7 oncogene mRNA detection was performed by NucliSens® EasyQ® HPV v1 Test (bioMérieux).ResultsThe results of the present study showed that E6/E7 mRNA positivity rate was 68.29 % in women tested once and 69.56 % in women tested twice. According to tissue pathology, all samples with high-grade lesions were positive for mRNA. Among women with low-grade lesions varied over the years from 89.28 to 84 % in women tested once and from 77.77 to 70 % in tested twice. Among women without lesion, positivity rate maintained in women tested once (from 50 to 41.38 %) and decreased in tested twice, from 63.63 to 44.44 %. Regarding lesion evolution, mRNA positivity was higher in women with lesion progression (53.13 %) and in women with positive results in two tested samples (83.33 %).ConclusionHPV E6/E7 mRNA detection may be an effective screening test and biomarker for cervical cancer in women infected with these five genotypes. Nonetheless, further studies are needed to standardize as routine triage test.

Pregnancy in women post-conization was associated with a risk of preterm delivery. However, there were no significant differences between women who underwent conization before and those who underwent conization after delivery. Cervical conization does not necessarily increase the risk of preterm delivery in subsequent pregnancy. Conization should be considered an indicator of such risk because it is associated with pregnancy complications arising from socio-epidemiologic factors present in women requiring conization that are also present in women who have premature delivery.

left cardiac output (CO) as determined by fetal Doppler studies. First trimester smoking, regardless of number of cigarettes smoked, showed no association with third trimester placental or fetal arterial resistance. For women who continued to smoke but smoked <5 cigarettes/d, no associations with fetal arterial resistance characteristics were seen. For mothers who smoked Z5 cigarettes/d throughout pregnancy, umbilical and uterine artery PI values and fetal middle cerebral artery PI were increased compared with nonsmokers. The fetuses of these mothers also had decreased ascending aorta diameter and ascending aorta peak systolic velocity and decreased left CO. Among mothers who continued to smoke, the largest decreases in third trimester estimated fetal weight and birth weight were associated with the highest umbilical artery resistances. The placental and fetal arterial resistance characteristics that were associated with maternal smoking were not associated with systolic and diastolic blood pressure or with left ventricular mass at age 2 years. An increased umbilical artery PI was associated with a reduced aortic root diameter, and an increased fetal middle cerebral artery PI was associated with a decreased ascending aorta diameter, left atrial diameter, and left CO at 2 years.In conclusion, this study found maternal smoking during pregnancy leads to fetal hemodynamic adaptations consistent with increased arterial resistance, which leads to fetal growth restriction and changes in postnatal cardiovascular development. Future studies are needed to determine if these adaptations may lead to the occurrence of cardiovascular disease later in life.