<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Sukowati, Caecilia H C</style></author><author><style face="normal" font="default" size="100%">Patti, Riccardo</style></author><author><style face="normal" font="default" size="100%">Pascut, Devis</style></author><author><style face="normal" font="default" size="100%">Ladju, Rusdina B</style></author><author><style face="normal" font="default" size="100%">Tarchi, Paola</style></author><author><style face="normal" font="default" size="100%">Zanotta, Nunzia</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author><author><style face="normal" font="default" size="100%">Tiribelli, Claudio</style></author><author><style face="normal" font="default" size="100%">Crocè, Lory S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Serum Stem Cell Growth Factor Beta for the Prediction of Therapy Response in Hepatocellular Carcinoma.</style></title><secondary-title><style face="normal" font="default" size="100%">Biomed Res Int</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Biomed Res Int</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Carcinoma, Hepatocellular</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemoembolization, Therapeutic</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Hematopoietic Cell Growth Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Liver Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasm Recurrence, Local</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">2018</style></volume><pages><style face="normal" font="default" size="100%">6435482</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;Introduction: &lt;/b&gt;Chronic inflammatory response is one of major contributors in the development of hepatocellular carcinoma (HCC). Inflammatory molecules, such as cytokines and growth factors in the circulation, can be useful in the diagnosis and prognosis of the patients. The stem cell growth factor beta (SCGF), a newly found protein, is a secreted sulfated glycoprotein and it functions as a growth factor for primitive hematopoietic progenitor cells. The level of SCGF had been reported to be elevated in several cancer types. However, there is very few or even no information on this protein in the study of HCC, even more in clinical studies.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Methods: &lt;/b&gt;A multiplex immunoassay panel of 48 cytokines and growth factors were utilized to screen 68 sera from 29 HCC patients at pretreatment (T0), 1 month (T1), and 6 months (T6) after treatment by either radiofrequency ablation (RF) or transarterial chemoembolization (TACE). Treatment response was evaluated according to mRECIST criteria.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Results: &lt;/b&gt;Immunoassay screening showed that the levels of IL-17, CTACK, TNF, IL-2R, IL-8, and SCGF were different in Complete Responders (CR) and Nonresponders (NR) groups. At T0 and T1, the SCGF level was significantly the highest in NR (23.8 and 40.7 ng/mL, respectively), followed by early recurrence (25.4 and 25.0 ng/mL), and CR (6.7 and 5.3 ng/mL), independently from HCV, stages, and treatment type. Low basal SCGF level was associated with longer disease-free survival compared to high SCGF.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Conclusion: &lt;/b&gt;In this study, for the first time, we demonstrate that the high level of serum SCGF at pre- and posttreatment is associated with HCC nonresponsiveness.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30246025?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Campisciano, Giuseppina</style></author><author><style face="normal" font="default" size="100%">Toschetti, Annamaria</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author><author><style face="normal" font="default" size="100%">Taranto, Rosanna Di</style></author><author><style face="normal" font="default" size="100%">Berton, Federico</style></author><author><style face="normal" font="default" size="100%">Stacchi, Claudio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Shifts of subgingival bacterial population after nonsurgical and pharmacological therapy of localized aggressive periodontitis, followed for 1 year by Ion Torrent PGM platform.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Dent</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur J Dent</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Jan-Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">11</style></volume><pages><style face="normal" font="default" size="100%">126-129</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The possibility of targeting the hypervariable region V3 of the 16S rRNA gene using Ion Torrent Personal Genome Machine (PGM) could provide a complete analysis of subgingival plaque samples, potentially able to identify microbiological species missed by culture-based methods. A 16-year-old female smoker patient, affected by localized aggressive periodontitis, underwent a full-mouth disinfection protocol and was inserted in a 3-month recall program. Microbiological samples were collected at baseline and at 30, 100, 365 days follow-up and analyzed by Ion Torrent PGM. , , , and  were the most represented pathogens at baseline. Nonsurgical treatment and systemic antibiotics drastically lowered the anaerobic species, and their presence remained limited after 100 days, while a consistent recolonization by anaerobic bacteria was detected at 365 days. The patient showed a general improvement of periodontal conditions. Differently from polymerase chain reaction and other microarray techniques, Ion Torrent performs a quantitative analysis of the microbiota, irrespective of the searched species. An accurate definition of the shifts of the bacterial community might help periodontal researchers for a better understanding of the impact of different treatment approaches or in intercepting nonresponsive conditions.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28435379?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Campisciano, Giuseppina</style></author><author><style face="normal" font="default" size="100%">Florian, Fiorella</style></author><author><style face="normal" font="default" size="100%">D'Eustacchio, Angela</style></author><author><style face="normal" font="default" size="100%">Stanković, David</style></author><author><style face="normal" font="default" size="100%">Ricci, Giuseppe</style></author><author><style face="normal" font="default" size="100%">De Seta, Francesco</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Subclinical alteration of the cervical-vaginal microbiome in women with idiopathic infertility.</style></title><secondary-title><style face="normal" font="default" size="100%">J Cell Physiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Cell. Physiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Biodiversity</style></keyword><keyword><style  face="normal" font="default" size="100%">Cervix Uteri</style></keyword><keyword><style  face="normal" font="default" size="100%">Cohort Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Demography</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infertility, Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Microbiota</style></keyword><keyword><style  face="normal" font="default" size="100%">Species Specificity</style></keyword><keyword><style  face="normal" font="default" size="100%">Vagina</style></keyword><keyword><style  face="normal" font="default" size="100%">Vaginosis, Bacterial</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">232</style></volume><pages><style face="normal" font="default" size="100%">1681-1688</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Biomarkers have a wide application in research and clinic, they help to choose the correct treatment for diseases. Recent studies, addressing the vaginal microbiome using next generation sequencing (NGS), reported the involvement of bacterial species in infertility. We compared the vaginal microbiome of idiopathic infertile women with that of healthy, including bacterial vaginosis affected women and non-idiopathic infertile women, to identify bacterial species suitable as biomarkers. Information on microorganisms was obtained from the V3-16S rDNA sequencing of cervical-vaginal fluids of 96 women using the Ion Torrent platform. Data were processed with QIIME and classified against the Vaginal 16S rDNA Reference Database. The analysis revealed a significant beta-diversity variation (p &lt; 0.001) between the four groups included in the study. L. iners, L. crispatus, and L. gasseri distinguished idiopathic infertile women from the other groups. In these women, a microbial profile similar to that observed in bacterial vaginosis women has been detected. Our results suggest that the quantitative assessment and identification of specific microorganisms of the cervical-vaginal microflora could increase the accuracy of available tools for the diagnosis of infertility and improve the adoption of therapeutic protocols.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">7</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28098358?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Cason, Carolina</style></author><author><style face="normal" font="default" size="100%">Campisciano, Giuseppina</style></author><author><style face="normal" font="default" size="100%">Zanotta, Nunzia</style></author><author><style face="normal" font="default" size="100%">Valencic, Erica</style></author><author><style face="normal" font="default" size="100%">Delbue, Serena</style></author><author><style face="normal" font="default" size="100%">Bella, Ramona</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">SV40 Infection of Mesenchymal Stromal Cells From Wharton's Jelly Drives the Production of Inflammatory and Tumoral Mediators.</style></title><secondary-title><style face="normal" font="default" size="100%">J Cell Physiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Cell. Physiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cell Line, Transformed</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Separation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Transformation, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokine CCL5</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokine CXCL9</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytopathogenic Effect, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Host-Pathogen Interactions</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation Mediators</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-12 Subunit p40</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-3</style></keyword><keyword><style  face="normal" font="default" size="100%">JC Virus</style></keyword><keyword><style  face="normal" font="default" size="100%">Mesenchymal Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Real-Time Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Simian virus 40</style></keyword><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Up-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Viral Load</style></keyword><keyword><style  face="normal" font="default" size="100%">Virus Replication</style></keyword><keyword><style  face="normal" font="default" size="100%">Wharton Jelly</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">232</style></volume><pages><style face="normal" font="default" size="100%">3060-3066</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The Mesenchymal Stromal Cells from umbilical cord Wharton's jelly (WJSCs) are a source of cells with high potentiality for the treatment of human immunological disorders. Footprints of the oncogenic viruses Simian Virus 40 (SV40) and JC Virus (JCPyV) have been recently detected in human WJSCs specimens. The aim of this study is to evaluate if WJSCs can be efficiently infected by these Polyomaviruses and if they can potentially exert tumoral activity. Cell culture experiments indicated that WJSCs could sustain both SV40 and JCPyV infections. A transient and lytic replication was observed for JCPyV, while SV40 persistently infected WJSCs over a long period of time, releasing a viral progeny at low titer without evident cytopathic effect (CPE). Considering the association between SV40 and human tumors and the reported ability of the oncogenic viruses to drive the host innate immune response to cell transformation, the expression profile of a large panel of immune mediators was evaluated in supernatants by the Bioplex platform. RANTES, IL-3, MIG, and IL-12p40, involved in chronic inflammation, cells differentiation, and transformation, were constantly measured at high concentration comparing to control. These findings represent a new aspect of SV40 biological activity in the humans, highlighting its interaction with specific host cellular pathways. In view of these results, it seems to be increasingly urgent to consider Polyomaviruses in the management of WJSCs for their safely use as promising therapeutic source. J. Cell. Physiol. 232: 3060-3066, 2017. © 2016 Wiley Periodicals, Inc.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">11</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27925194?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Mazzoni, Elisa</style></author><author><style face="normal" font="default" size="100%">Rigolin, Gian Matteo</style></author><author><style face="normal" font="default" size="100%">Alaribe, Franca Nneka</style></author><author><style face="normal" font="default" size="100%">Pancaldi, Cecilia</style></author><author><style face="normal" font="default" size="100%">Maniero, Stefania</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author><author><style face="normal" font="default" size="100%">Martini, Fernanda</style></author><author><style face="normal" font="default" size="100%">Tognon, Mauro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Simian virus 40 efficiently infects human T lymphocytes and extends their lifespan.</style></title><secondary-title><style face="normal" font="default" size="100%">Exp Hematol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Exp. Hematol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Antigens, Polyomavirus Transforming</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line, Transformed</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Microscopy, Electron, Transmission</style></keyword><keyword><style  face="normal" font="default" size="100%">Simian virus 40</style></keyword><keyword><style  face="normal" font="default" size="100%">T-Lymphocytes</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">40</style></volume><pages><style face="normal" font="default" size="100%">466-76</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The relevance of viral infections to the onset and progression of human hematologic malignancies and other blood diseases is still a matter of active investigation. Purified human T lymphocytes isolated from the peripheral blood mononuclear cells of healthy blood donors were experimentally infected with simian virus 40 (SV40), a small DNA tumor virus. SV40-positive T lymphocytes extended their lifespan up to day 80 postinfection (PI). Expression of viral antigens, such as the large T antigen and the viral capsid protein VP1 from the early and late regions, respectively, was detected up to day 40 PI. SV40 viral progeny were continuously produced from day 10 to 40 PI. SV40 DNA sequences were detected in infected T cells for up to 80 days. Our data indicate that human T lymphocytes can be efficiently infected with SV40. Although T cells infected by SV40 were not immortalized, 30% of these lymphocytes appeared to be morphologically transformed with an enlarged T-cell shape. Our investigation provides a simple model for studying the interactions of human T lymphocytes with this small DNA tumor virus and it might represent an experimental tool for investigating new biomarkers and targets for innovative therapeutic approaches.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22421183?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zanin, Valentina</style></author><author><style face="normal" font="default" size="100%">Delbue, Serena</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author><author><style face="normal" font="default" size="100%">Tavazzi, Eleonora</style></author><author><style face="normal" font="default" size="100%">Del Savio, Rossella</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Marchioni, Enrico</style></author><author><style face="normal" font="default" size="100%">Ferrante, Pasquale</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Specific protein profile in cerebrospinal fluid from HIV-1-positive cART-treated patients affected by neurological disorders.</style></title><secondary-title><style face="normal" font="default" size="100%">J Neurovirol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Neurovirol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Anti-HIV Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Encephalomyelitis, Acute Disseminated</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV-1</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukoencephalopathy, Progressive Multifocal</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Pilot Projects</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">18</style></volume><pages><style face="normal" font="default" size="100%">416-22</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Cytokines/chemokines are involved in the immune response of infections, including HIV-1. We defined the profile of 48 cytokines/chemokines in cerebrospinal fluid from 18 cART patients with chronic HIV-1 infection by Luminex technology. Nine patients were affected with leukoencephalopathies: five with John Cunningham virus (JCV) + progressive multifocal leukoencephalopathy (PML) and four with JCV-not determined leukoencephalopathy (NDLE). In addition, nine HIV-1-positive patients with no neurological signs (NND) and five HIV-1-negative patients affected with acute disseminated encephalomyelitis (ADEM) were enrolled. Ten cytokines (IL-15, IL-3, IL-16, IL-18, CTACK, GRO1, SCF, MCP-1, MIF, SDF) were highly expressed in HIV-1-positive patients while IL-1Ra and IL-17 were present at a lower level. In addition, the levels of IL-17, IL-9, FGF-basic, MIP-1β, and MCP-1 were significantly higher (p &lt; 0.05) in patients with neurological diseases (PML, NDLE, ADEM) with respect to NND. Focusing the attention to the cytokine profile in JCV + PML patients with respect to JCV-NDLE patients, only TNF-β was significantly downregulated (p &lt; 0.05) in JCV + PML patients. This pilot study emphasized the role of immunoregulation in HIV-1-related neurological disorders during cART treatment.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22581428?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Comar, Manola</style></author><author><style face="normal" font="default" size="100%">Zanotta, Nunzia</style></author><author><style face="normal" font="default" size="100%">Rossi, Tatiana</style></author><author><style face="normal" font="default" size="100%">Pelos, Giorgio</style></author><author><style face="normal" font="default" size="100%">D'Agaro, Pierlanfranco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Secondary lymphoid tissue as an important site for WU polyomavirus infection in immunocompetent children.</style></title><secondary-title><style face="normal" font="default" size="100%">J Med Virol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Med. Virol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adenoids</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukocytes, Mononuclear</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Nasopharynx</style></keyword><keyword><style  face="normal" font="default" size="100%">Palatine Tonsil</style></keyword><keyword><style  face="normal" font="default" size="100%">Phylogeny</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Polyomavirus</style></keyword><keyword><style  face="normal" font="default" size="100%">Polyomavirus Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Prevalence</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Analysis, DNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Homology</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">83</style></volume><pages><style face="normal" font="default" size="100%">1446-50</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The polyomaviruses KI and WU (KIPyV and WUPyV) have been identified in respiratory specimens from children with acute respiratory infections, which suggests the respiratory tract as a possible site of infection. However, the persistence of infection in the lymphoid system is unknown. Fresh samples (n = 211) of tonsils, adenoids, and peripheral blood mononuclear cells (PBMCs) from 83 immunocompetent children (mean age 4.8 years) were tested for amplification of the KIPyV VP1 and WUPyV VP2 genes. The known BK and JC polyomaviruses and the lymphotropic human herpesvirus (HHV)-6 were also investigated by quantitative real-time PCR and direct sequencing. In addition, 98 nasopharyngeal swabs collected from children (mean age 6.2 years) affected by seasonal influenza-like illness were tested. Of the lymphoid tissues, 34.9% were positive for WUPyV, 4.8% for BK virus, and 33.8% for HHV-6. KIPyV and JC virus were not detected in these specimens. None of the polyomaviruses were detected in PBMCs. Among the nasopharyngeal samples, the prevalence of WUPyV was 27.5%, although 70% of the positive samples were co-infected with at least one of the following respiratory viruses: influenza virus, adenovirus, and respiratory syncytial virus. Phylogenetic analysis revealed high sequence homology (99%) between lymphoid- and nasopharynx-derived WUPyV strains. These results suggest that the tonsils and adenoids of immunocompetent children are a reservoir for WUPyV infection; probably due to the respiratory route of transmission. In addition, the prevalence of WUPyV was high among the children, and the virus was identified more frequently in older children than during the first years of life.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">8</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21678449?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Comar, Manola</style></author><author><style face="normal" font="default" size="100%">Segat, Ludovica</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Bovenzi, Massimo</style></author><author><style face="normal" font="default" size="100%">Cortini, Enzo</style></author><author><style face="normal" font="default" size="100%">Tognon, Mauro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The significance of mannose-binding lectin gene polymorphisms on the risk of BK virus coinfection in women with human papillomavirus-positive cervical lesions.</style></title><secondary-title><style face="normal" font="default" size="100%">Hum Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Hum. Immunol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">BK Virus</style></keyword><keyword><style  face="normal" font="default" size="100%">Cervical Intraepithelial Neoplasia</style></keyword><keyword><style  face="normal" font="default" size="100%">Cervix Uteri</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Fingerprinting</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Frequency</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Association Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Human papillomavirus 16</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Mannose-Binding Lectin</style></keyword><keyword><style  face="normal" font="default" size="100%">Odds Ratio</style></keyword><keyword><style  face="normal" font="default" size="100%">Papillomavirus Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Polyomavirus Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk</style></keyword><keyword><style  face="normal" font="default" size="100%">Viral Load</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">72</style></volume><pages><style face="normal" font="default" size="100%">663-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The simultaneous detection of oncogenic human papillomavirus (HPV) and BK virus (BKV) has been recently reported in cervical cancers, suggesting that these viruses may act together in the process of cell transformation; host genetic polymorphisms may also influence virus persistence/reactivation. To disclose a possible role of the gene encoding for the mannose-binding lectin, MBL2, in susceptibility to BKV infection, we analyzed functional polymorphisms in the first exon of MBL2 in women stratified for the presence/absence of BKV and affected by different grades of HPV-induced cervical precancerous lesions. All BKV-positive samples were also HPV positive (HPV 16), and all presented with high-grade squamous intraepithelial lesions. The MBL2 A allele was significantly more frequent in BKV-negative patients than in BKV-positive patients. These data indicate a possible role for the A allele in conferring protection to BKV infection in high-risk HPV-positive women (odds ratio 0.40, 95% confidence interval 0.20-0.85, p = 0.01).&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">8</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21536088?dopt=Abstract</style></custom1></record></records></xml>