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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.journalofclinicalvirology.com/?rss=yes"><title>Journal of Clinical Virology</title><description>Journal of Clinical Virology RSS feed: Current Issue. 
 Journal of Clinical Virology  is an international journal publishing papers on any aspect of human virology that directly pertains 
to virus-induced clinical conditions under the major headings of: Epidemiology, Pathogenesis, Diagnosis and Detection, and Prevention 
and Treatment. Articles from any field of virological study will be considered if the article is relevant to the understanding or manipulation 
of a disease state.</description><link>http://www.journalofclinicalvirology.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:issn>1386-6532</prism:issn><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:publicationDate>February 2010</prism:publicationDate><prism:copyright> © 2010 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209006313/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS138665320900479X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005320/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005332/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005629/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005599/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005587/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005575/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS138665320900571X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005563/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005708/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005642/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS138665320900554X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005526/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005630/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005691/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS138665320900568X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005654/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005605/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005435/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005502/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005666/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209005617/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653209006349/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209006313/abstract?rss=yes"><title>Editorial Board</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209006313/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1386-6532(09)00631-3</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>iii</prism:startingPage><prism:endingPage>iii</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS138665320900479X/abstract?rss=yes"><title>Severe gastroenteritis with secondary fever in a 10-month-old boy</title><link>http://www.journalofclinicalvirology.com/article/PIIS138665320900479X/abstract?rss=yes</link><description>A 10-month-old boy presented in our emergency department in a severely reduced general condition, apathetic and sleepy. He had non-bloody diarrhea and had been vomiting for two days prior to admission. As medication he did receive dimenhydrinate, which did not improve his symptoms. His mother also had diarrhea at the same time. Beginning at the evening before admission to our hospital he refused eating and drinking. At 3am on the day of admission his mother found him in a stuporous state, not reacting properly. Consequently he was brought to the hospital. Until that day the patient had developed regularly and was otherwise well. In the emergency room he did not react much to stimulation and often fell asleep. The examination revealed a heavily inflated abdomen. There was no pain during palpation, no enlargement of liver and spleen, no resistance.</description><dc:title>Severe gastroenteritis with secondary fever in a 10-month-old boy</dc:title><dc:creator>Stephanie Schenk, Angela Petzold, Marina Hoehne, Rüdiger Adam, Horst Schroten, Tobias Tenenbaum</dc:creator><dc:identifier>10.1016/j.jcv.2009.09.031</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-10-30</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-10-30</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Virology Question and Answer Scheme (VIROQAS)</prism:section><prism:startingPage>107</prism:startingPage><prism:endingPage>109</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005320/abstract?rss=yes"><title>Crimean-Congo hemorrhagic fever in Iran and neighboring countries</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005320/abstract?rss=yes</link><description>Abstract: Crimean-Congo hemorrhagic fever (CCHF) is a zoonotic viral disease that is asymptomatic in infected livestock, but a serious threat to humans. Human infections begin with nonspecific febrile symptoms, but progress to a serious hemorrhagic syndrome with a case fatality rate of 2–50%. Although the causative virus is often transmitted by ticks, livestock-to-human and human-to-human transmissions also occur. The disease is one of the most widely distributed viral hemorrhagic fevers occurring in Africa, the Middle East, Asia, and some parts of Europe. In this study, we have focused on the CCHF situation in Iran and neighboring countries and provide evidence of over 5000 confirmed cases of CCHF in a single period/season.</description><dc:title>Crimean-Congo hemorrhagic fever in Iran and neighboring countries</dc:title><dc:creator>S. Chinikar, S.M. Ghiasi, R. Hewson, M. Moradi, A. Haeri</dc:creator><dc:identifier>10.1016/j.jcv.2009.10.014</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-14</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-14</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Review</prism:section><prism:startingPage>110</prism:startingPage><prism:endingPage>114</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005332/abstract?rss=yes"><title>Evaluation of the association of serum levels of hyaluronic acid, sICAM-1, sVCAM-1, and VEGF-A with mortality and prognosis in patients with Crimean-Congo hemorrhagic fever</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005332/abstract?rss=yes</link><description>Abstract: Background: Crimean-Congo hemorrhagic fever (CCHF) is a tick-borne viral hemorrhagic disease. Pathogenesis of the disease has not been well described yet. A well-known pathogenic feature of CCHF virus is its capability to damage endothelium. Increased hyaluronic acid (HA) levels indicate liver sinusoidal endothelial damage. Soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and vascular endothelial growth factor-A (VEGF-A) play a role in the inflammatory process, vascular damage and plasma leakage.Objectives: To investigate whether or not there is a relationship between HA, sICAM-1, sVCAM-1 and VEGF-A serum levels and fatality in CCHF.Study design: Sixty-one patients who were confirmed by RT-PCR and serological tests for CCHF, included in the current study. HA, sICAM-1, sVCAM-1, VEGF-A levels in serum samples were analyzed by ELISA.Results: There were statistically significant differences between fatal and non-fatal CCHF patients in terms of HA, sICAM-1, sVCAM-1, and VEGF-A levels. In addition, AST and ALT levels were positively correlated with HA, sICAM-1, sVCAM-1, and VEGF-A levels.Conclusion: HA, sICAM-1, sVCAM-1, and VEGF-A levels of the patients that died during hospitalization were statistically significantly higher than the patients that survived, and this finding suggests that the level of these molecules could be used as a prognostic marker in CCHF.</description><dc:title>Evaluation of the association of serum levels of hyaluronic acid, sICAM-1, sVCAM-1, and VEGF-A with mortality and prognosis in patients with Crimean-Congo hemorrhagic fever</dc:title><dc:creator>Baris Ozturk, Ferit Kuscu, Ediz Tutuncu, Irfan Sencan, Yunus Gurbuz, Hakan Tuzun</dc:creator><dc:identifier>10.1016/j.jcv.2009.10.015</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-11</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-11</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>115</prism:startingPage><prism:endingPage>119</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005629/abstract?rss=yes"><title>Measuring human immunodeficiency virus type 1 RNA loads in dried blood spot specimens using NucliSENS EasyQ HIV-1 v2.0</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005629/abstract?rss=yes</link><description>Abstract: Background: HIV-1 RNA plasma level is a key parameter for anti-viral treatment monitoring in HIV-1 infected individuals. Plasma stability and accurate measurement of clinical state is at risk when transporting from remote areas. Dried blood spot (DBS) testing can reduce this risk.Objectives: Determine the performance of NucliSENS EasyQ HIV-1 v2.0 for DBS.Study design: 100 HIV-1 negative, and 129 HIV-1 spiked blood specimens (2180copies/ml) were used for diagnostic specificity and system robustness. Analytical performance was tested in the range 50–85,000,000copies/ml. Clinical reactivity was measured with specimens obtained from 224 HIV-1 infected individuals. HIV-1 RNA stability was analyzed after applying several different storage conditions.Results: Diagnostic specificity was 100% and system robustness was demonstrated by 100% detection rate without invalids. Limit of detection (95% detection rate) was 800copies/ml. Linear results were obtained over the whole range tested. For clinical specimens, percentage positive results were comparable for DBS (57%) and plasma (58%). DBS quantification was on average 0.36log10 lower as compared to plasma. Specimen stability was demonstrated for 1 week at 55°C/60% humidity, 3 weeks at 37°C/80% humidity, 9 weeks at 37°C/40% humidity, 3 months at −20°C/70% humidity, 3 weeks at 4°C/100% humidity, 9 months at room temperature (15–30°C), and 9 weeks shipment simulation.Conclusion: Results obtained fully support the use of DBS for the NucliSENS EasyQ HIV-1 v2.0 assay. These findings are especially of importance in cases that plasma stability is currently at risk due to for example, long transport routes from remote areas under less controlled conditions.</description><dc:title>Measuring human immunodeficiency virus type 1 RNA loads in dried blood spot specimens using NucliSENS EasyQ HIV-1 v2.0</dc:title><dc:creator>Peter van Deursen, Tom Oosterlaken, Patrice Andre, André Verhoeven, Lieke Bertens, Mary Anne Trabaud, Veronique Ligeon, Jacques de Jong</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.021</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-18</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-18</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>120</prism:startingPage><prism:endingPage>125</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005599/abstract?rss=yes"><title>Development and performance of a new recombinant virus phenotypic entry assay to determine HIV-1 coreceptor usage</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005599/abstract?rss=yes</link><description>Abstract: Background: Clinical trials of CCR5 antagonists have relied on the phenotypic determination of HIV-1 coreceptor usage. Few phenotypic assays are available, with few data on their concordance, and none has been designed to determine tropism from cell-associated HIV-1 DNA.Objectives: To assess the performance of the new Toulouse Tropism Test (TTT) phenotypic assay to characterize HIV-1 tropism using blood plasma and peripheral blood mononuclear cells (PBMC).Study design: 434 plasma and 168 PBMC samples were tested with the TTT assay. We determined the correlation between our assay results on plasma samples and those of the commercial Trofile™ assay.Results: The TTT assay determined the tropism of 97% of samples after successful amplification of the env gene. It performed well on both cell samples and plasma samples with various HIV-1 loads and subtypes. It detected 0.5% of minor CXCR4-using variants in the virus population. The TTT and the Trofile™ assays were &gt;90% concordant for predicting HIV-1 tropism.Conclusion: We have validated a new recombinant virus phenotypic assay for determining HIV-1 tropism using both plasma and cell samples from patients who are candidates for treatment with CCR5 antagonists.</description><dc:title>Development and performance of a new recombinant virus phenotypic entry assay to determine HIV-1 coreceptor usage</dc:title><dc:creator>Stéphanie Raymond, Pierre Delobel, Maud Mavigner, Michelle Cazabat, Corinne Souyris, Stéphanie Encinas, Patrick Bruel, Karine Sandres-Sauné, Bruno Marchou, Patrice Massip, Jacques Izopet</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.018</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-16</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-16</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>126</prism:startingPage><prism:endingPage>130</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005587/abstract?rss=yes"><title>The prognosis of highly active antiretroviral therapy (HAART) treated HIV infected patients in Serbia, related to the time of treatment initiation</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005587/abstract?rss=yes</link><description>Abstract: Background: With the introduction of highly active antiretroviral treatment (HAART) an impressive improvement in patient survival and quality of life has bee observed. However, the optimal timing of initial HAART is still under consideration.Objective: To investigate the prognosis of HAART treated patients in Serbia, related to the timing of HAART initiation.Study design: A series of 563 patients on HAART was retrospectively analyzed to investigate treatment response and survival.Results: After a mean of 6 years (range 1–14) of treatment with PI-based and/or NNRTI-based regimens, a favorable response was achieved in 72.4%, treatment failure occurred in 7.9%, while 19.7% had a dissociative immunological/virological response. If treatment was initiated during primary HIV infection it took a shorter time to achieve a favorable response than in patients who began HAART in chronic HIV infection (2.7±2.2 years vs. 6.9±2.7 years, P&lt;0.01). A higher proportion of patients with primary HIV infection then those treated in the chronic phase achieved a favorable response to HAART (88.4% vs. 71.9%, P=0.045). Patients who initiated HAART when their CD4 cell counts were below 200cells/μL needed longer treatment for favorable response (8 years vs. 6 years, log rank P&lt;0.01). Forty-seven (8.3%) patients died. The overall estimated survival was 13 years. Patients older then 40 and IVDU were more likely to die during HAART (OR 2.6, 95% CI 1.1–5.9, P=0.016, and OR 2.0, 95% CI 1.0–3.7, P=0.02, respectively). However, reaching and maintaining undetectable viremia was an independent predictor of longer survival (OR 11.3, 95% CI 4.6–27.7, P&lt;0.01).Conclusion: Reaching and maintaining undetectable viremia during HAART predicted longer survival, even if sub-clinical immunodeficiency remained.</description><dc:title>The prognosis of highly active antiretroviral therapy (HAART) treated HIV infected patients in Serbia, related to the time of treatment initiation</dc:title><dc:creator>Dj. Jevtović, D. Salemović, J. Ranin, O. Dulović, D. Ilić, B. Brmbolić</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.017</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-14</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-14</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>131</prism:startingPage><prism:endingPage>135</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005575/abstract?rss=yes"><title>The prevalence of human endogenous retroviruses in cerebrospinal fluids from patients with sporadic Creutzfeldt–Jakob disease</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005575/abstract?rss=yes</link><description>Abstract: Background: About 8% of human genome is constituted by retroviral sequences. Some of these have been classified as human endogenous retroviruses (HERVs), which have been implicated in both health and disease. Recently, indirect evidence for a possible role of retroviral elements in neurological diseases has been provided by several studies.Objectives: In the present study, we aimed to evaluate the relationship between HERVs and sporadic Creutzfeldt–Jakob disease (CJD), one of the human forms of prion diseases.Study design: We investigated the prevalence of HERV families by RT-PCR in cell-free cerebrospinal fluids (CSFs) samples from normal controls, patients with sporadic CJD and other neurological diseases (OND).Results: The incidence rate of some HERV families were significantly different in CSF samples from the group of sporadic CJD compared to samples from normal individuals; HERV-W (P=0.001), T (P=0.039), FRD (P&lt;0.001), L (P=0.003) and ERV-9 (P&lt;0.001) and the incidence rate of HERV-W (P=0.021) and HERV-L (P=0.049) were significantly increased in CSF samples from the group of sporadic CJD compared to samples from OND group. Moreover, our results from combining frequencies of two HERV families indicated that the prevalence of many combination groups was significantly different between sporadic CJD and normal CSF samples and between two patients’ CSF samples. In addition, a large number of HERV sequences were newly identified in CSFs from normal and diseased individuals.Conclusions: Our study about distinct prevalence patterns of HERVs reflects that some HERVs families may be associated with the development of prion diseases, and considered as a candidate marker for the diagnosis of sporadic CJD.</description><dc:title>The prevalence of human endogenous retroviruses in cerebrospinal fluids from patients with sporadic Creutzfeldt–Jakob disease</dc:title><dc:creator>Byung-Hoon Jeong, Yun-Jung Lee, Richard I. Carp, Yong-Sun Kim</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.016</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-11</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-11</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>136</prism:startingPage><prism:endingPage>142</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS138665320900571X/abstract?rss=yes"><title>Newly recognized bocaviruses (HBoV, HBoV2) in children and adults with gastrointestinal illness in the United States</title><link>http://www.journalofclinicalvirology.com/article/PIIS138665320900571X/abstract?rss=yes</link><description>Abstract: Background: The human bocavirus (HBoV) is a newly recognized parvovirus associated with respiratory and gastrointestinal disease. Recently, two new members of the parvovirus family have been recognized, HBoV2 and HBoV3.Objectives: Here we investigate stool and respiratory samples for the presence of HBoV, HBoV2 and HBoV3.Study design: Stool samples collected from 12/1/2007 to 3/31/2008 were screened by PCR for the presence of HBoV, HBoV2, and HBoV3. Extracted DNA from respiratory specimens archived between 10/17/2005 and 3/29/2006 were screened by PCR for HBoV2 and HBoV3. Medical records for all bocavirus positive patients were reviewed.Results: Of 479 stool samples screened, 328 (68.5%) were from adults, and 151 (31.5%) were from children. Sixteen (3.4%) patients were positive for the presence of a bocavirus, including 10 (2.1%) HBoV and 6 (1.3%) HBoV2. No HBoV3 was detected in stool samples. Frequency of HBoV and HBoV2 in stool samples from children was 3.3% and 0.7%, and from adults was 1.5% and 1.5% respectively. Clinical findings in patients with HBoV and HBoV2 in stool include diarrhea (50% and 83.3%), abdominal pain (40%, 33.3%), and cough (10%, 50%). Of 868 respiratory samples screened, none were positive for either HBoV2 or HBoV3.Conclusions: The newly recognized parvovirus HBoV2 circulates in the United States. Patients with bocaviruses in stool have evidence of gastrointestinal illness. HBoV2 was not detected in respiratory samples. HBoV3 was not detected in either stool or respiratory samples.</description><dc:title>Newly recognized bocaviruses (HBoV, HBoV2) in children and adults with gastrointestinal illness in the United States</dc:title><dc:creator>Brian D.W. Chow, Zhen Ou, Frank P. Esper</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.030</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-28</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-28</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>143</prism:startingPage><prism:endingPage>147</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005563/abstract?rss=yes"><title>Correlation between bocavirus infection and humoral response, and co-infection with other respiratory viruses in children with acute respiratory infection</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005563/abstract?rss=yes</link><description>Abstract: Background: Human bocavirus (HBoV), a recently discovered virus, is prevalent among children with respiratory tract infection throughout the world. Co-infection was frequently found in HBoV-positive patients. Thus, whether HBoV is responsible for the respiratory disease is still arguable.Objectives: A comprehensive study was carried out to integrate clinical and virological prevalence in HBoV-positive outpatient children, and to determine genetic and serologic characteristics of HBoV in Shanghai, China.Study design: Nasal/throat swabs and sera were obtained over a 2-year period from 817 children with respiratory tract infection to examine the presence of HBoV and its co-infection. The seroepidemiology of HBoV was studied by ELISA and Western blot against the capsid protein VP2-based fragment. Persistence of HBoV was also analyzed in 12 pairs of return-visit cases.Results: HBoV was identified in 96 samples (11.8%). The co-infection rate with other respiratory viruses was 51%. IgM was detected in 55.7% of HBoV RT-PCR-positive patients, and in 72.7% of those who had high viral genome load. In addition, persistent viral DNA positivity was detected in 10 of 12 HBoV-positive cases tested, an average of 14 days later, and one child was still HBoV-positive after 31 days.Conclusion: HBoV was found frequently in children with respiratory tract symptoms associated with other respiratory viruses, and persisted in the respiratory tract and in serum and urine. The presence of IgM was significantly more prevalent in viremic patients and those diagnosed with high load of HBoV DNA in nasal/throat swabs.</description><dc:title>Correlation between bocavirus infection and humoral response, and co-infection with other respiratory viruses in children with acute respiratory infection</dc:title><dc:creator>Kai Wang, Wei Wang, Huajie Yan, Peijun Ren, Jing Zhang, Jun Shen, Vincent Deubel</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.015</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-18</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-18</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>148</prism:startingPage><prism:endingPage>155</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005708/abstract?rss=yes"><title>Lymphotropic Polyomavirus is detected in peripheral blood from immunocompromised and healthy subjects</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005708/abstract?rss=yes</link><description>Abstract: Background: Lymphotropic Polyomavirus (LPV) was isolated from a B-lymphoblastoid cell line of an African green monkey. This virus shares some characteristics with human polyomaviruses, but it is antigenically distinct from BK Virus (BKV) and JC Virus (JCV). Seroepidemiological studies revealed that human sera react in the presence of LPV antigens, and, recently, the viral genome was amplified in the peripheral blood from patients affected with HIV-related leukoencephalopathies.Objectives: The aims of the study were to investigate and compare the presence of LPV DNA with that of JCV and BKV in different biological samples and patient groups.Study design: LPV, JCV and BKV DNA were searched and quantified in peripheral blood and CSF from HIV+ patients and in peripheral blood from healthy subjects.Results: The LPV genome was detected in peripheral blood of both HIV+ patients and healthy subjects, with a prevalence of 7.2% and 4.7% respectively, but not in CSF. However, its presence was less frequent than that of JCV and BKV.Conclusions: The amplification of LPV genome from human peripheral blood confirms the fact that LPV can infect the human population. LPV DNA was amplified from patients affected with HIV-related leukoencephalopathies but also from HIV patients without neurological disorders and from healthy subjects. Therefore, the results do not support the hypothesis of an association between LPV infection and any neurological disease. However, given their high similarity, it is possible that LPV, as well as BKV and JCV, could establish latency in humans and cause disease only in rare circumstances.</description><dc:title>Lymphotropic Polyomavirus is detected in peripheral blood from immunocompromised and healthy subjects</dc:title><dc:creator>Serena Delbue, Sara Tremolada, Francesca Elia, Camilla Carloni, Serena Amico, Eleonora Tavazzi, Enrico Marchioni, Stefano Novati, Renato Maserati, Pasquale Ferrante</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.029</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-30</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-30</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>156</prism:startingPage><prism:endingPage>160</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005642/abstract?rss=yes"><title>Variability and recombination of clinical human cytomegalovirus strains from transplantation recipients</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005642/abstract?rss=yes</link><description>Abstract: Background: Human cytomegalovirus (HCMV) is the first cause of viral infection in immunocompromised transplanted patients.Objectives: Here, five HCMV genes were studied to investigate the existence of recombination events in clinical strains ex vivo.Study design: Sequencing and phylogenetic analysis were conducted on 21 strains from 16 renal and 5 lung transplant recipients.Results: Nucleotidic polymorphism ranged from 6.6% (US3) to 12% (UL40), with a significant proportion of missense mutations (39–69%), some of which could have a functional impact. Analysis of the concatenated sequence (4804 nucleotides for each strain) evidenced two clusters of sequences presenting a reticulate topology suggestive of recombination events (SplitsTree). Phi-test pointed numerous phylogenetically conflicting signals indicating a high statistical probability of recombination. The subsequent bootscan analysis was consistent with these data.Conclusions: These results reinforce the prominent role of recombination in HCMV evolutionary history and adaptation to its host.</description><dc:title>Variability and recombination of clinical human cytomegalovirus strains from transplantation recipients</dc:title><dc:creator>Muriel Faure-Della Corte, Johan Samot, Isabelle Garrigue, Noël Magnin, Sandrine Reigadas, Lionel Couzi, Claire Dromer, Jean-François Velly, Julie Déchanet-Merville, Hervé J.A. Fleury, Marie-Edith Lafon</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.023</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-18</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-18</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>161</prism:startingPage><prism:endingPage>169</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS138665320900554X/abstract?rss=yes"><title>Enteroviruses in Spain over the decade 1998–2007: Virological and epidemiological studies</title><link>http://www.journalofclinicalvirology.com/article/PIIS138665320900554X/abstract?rss=yes</link><description>Abstract: Background: Human enteroviruses (HEV) are the commonest cause of viral meningitis as well as other pathologies, therefore HEV characterization is important both in patient management and epidemiological investigation.Objectives: A 10-year study of patients with enteroviral infection was carried out in Spain to determine the underlying etiology.Study design: HEV were fully typed by microneutralisation tests and/or molecular methods.Results: A collection of 86404 clinical samples were studied in several Spanish laboratories. These were collected from patients with different syndromes, mainly aseptic meningitis (AM), fever, respiratory diseases and acute flaccid paralysis. Of these, 6867 HEV were obtained. At the National Poliovirus Laboratory 2814 were serotypically characterised. Among non-polio enteroviruses, the eight main serotypes were Echovirus 30 (25%), Echovirus 6 (12.4%), Echovirus 13 (8.3%), Echovirus 11 (7.4%) and Echovirus 9 (4.7%), followed by Coxsackievirus B5 (4.2%) and Echovirus 7 and Coxsackievirus A9 (3.7%) each. In AM cases, Echovirus 30 was identified in 39% of them, followed by Echovirus 6 (14%). However, Echovirus 6 was mainly associated with respiratory disease (17%), followed by Echovirus 11 (10%). On the other hand, Echovirus 30, Echovirus 11 and Echovirus 6 contributed equally with 12% of each serotype in the cases of fever.Conclusions: The present report complements previous data (Trallero et al.), with the results of HEV incidence in Spain from 1998 to 2007. The surveillance described in this study provided valuable information as to which serotypes are in circulation, the emergence of new HEV and association with clinical manifestations.</description><dc:title>Enteroviruses in Spain over the decade 1998–2007: Virological and epidemiological studies</dc:title><dc:creator>G. Trallero, A. Avellon, A. Otero, T. De Miguel, C. Pérez, N. Rabella, G. Rubio, J.E. Echevarria, M. Cabrerizo</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.013</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-15</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-15</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>170</prism:startingPage><prism:endingPage>176</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005526/abstract?rss=yes"><title>Relevance of HPV mRNA detection in a population of ASCUS plus women using the NucliSENS EasyQ® HPV assay</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005526/abstract?rss=yes</link><description>Summary: Background: DNA- and mRNA-based assays are the main tools used for detecting human papillomavirus (HPV) nucleic acid in clinical samples. A recent tool, NucliSENS EasyQ HPV, uses a new concept to directly detect the expression of HPV oncogenic factors (E6 and E7) from the most prevalent HPV genotypes in cervical cancer (16, 18, 31, 33 and 45).Objectives: The primary aim of the study is to assess the accuracy of NucliSENS EasyQ HPV in detecting high-risk (HR) HPV in a population of atypical cells of undetermined significance/low-grade squamous intraepithelial lesion/high-grade squamous lesion (ASCUS/LSIL/HSIL) patients using a clinical cut-off of a cervical dysplasia (CIN2+) histology. The secondary aim is to compare this mRNA-based assay with the DNA-based hybrid capture II (HCII) assay.Study design: The study population comprised 140 women referred for colposcopy and histology. NucliSENS EasyQ HPV test, hybrid capture II (HCII) test and linear array (LA) test were assessed on all samples. All the tests were performed on the samples collected in PreservCyt liquid media for liquid-based cytology (ThinPrep Pap test).Results: The clinical specificity of the NucliSENS EasyQ HPV was 63% for the detection of CIN2+ or HSIL patients, significantly higher than the specificity of HCII and LA (49% and 45%, respectively, p&lt;0.05). Agreement between HCII and NucliSENS EasyQ HPV was fair (k=0.49) and was good between HCII and LA (k=0.88). HPV 16 was the most-detected type (49% with NucliSENS EasyQ HPV and 56% with LA), and HPV 31 was the second most-detected HPV type (31% with NucliSENS EasyQ HPV and 29% with LA).Conclusions: The NucliSENS EasyQ HPV assay has interesting clinical sensitivity and specificity for the detection of HPV types in CIN2+ patients and shows comparable diagnostic values with the HCII DNA assay. This assay allows simultaneous detection of HPV mRNA and determination of the type of the main prevalent oncogenic virus.</description><dc:title>Relevance of HPV mRNA detection in a population of ASCUS plus women using the NucliSENS EasyQ® HPV assay</dc:title><dc:creator>Philippe Halfon, Dominique Benmoura, Aubert Agostini, Hacene Khiri, Agnés Martineau, Guillaume Penaranda, Bernard Blanc</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.011</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-21</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-21</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>177</prism:startingPage><prism:endingPage>181</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005630/abstract?rss=yes"><title>Performance of laboratory diagnostics for the detection of influenza A(H1N1)v virus as correlated with the time after symptom onset and viral load</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005630/abstract?rss=yes</link><description>Abstract: Background: To diagnose influenza A(H1N1)v virus infection, accurate and rapid detection are important. However, there is scanty data on the performance of various laboratory diagnostics.Objective: To compare the performance of rapid antigen test (RAT), viral culture and RT-PCR for the detection of influenza A(H1N1)v virus and to correlate their performance with the time after symptom onset and viral load.Study Design: From May 1, 2009 to June 25, 2009, respiratory samples were collected from 5740 individuals suspected of having influenza A(H1N1)v infection. The performance of viral culture and RT-PCR were investigated and correlated with the time after symptom onset. The sensitivity of RAT ESPLINE influenza A &amp; B-N (Fujirebio Inc, Tokyo) was evaluated using a subset of 60 samples from patients diagnosed as having influenza A(H1N1)v infection.Results: Using respiratory samples from 587 patients diagnosed with influenza A(H1N1)v infection, comparison of laboratory diagnostics showed viral culture and RT-PCR gave comparable results with overall sensitivity of 93.9% and 98.1%, respectively. For RAT, when testing a subset of 60 samples collected ≤3 days following symptom onset, the sensitivity was 62%.Conclusions: Although viral shedding is prolonged and of higher titre in influenza A(H1N1)v infection, RAT showed a low sensitivity of 62% among patients presenting ≤3 days after symptom onset. Viral culture showed comparable performance with RT-PCR and with sensitivity better than that documented for seasonal influenza.</description><dc:title>Performance of laboratory diagnostics for the detection of influenza A(H1N1)v virus as correlated with the time after symptom onset and viral load</dc:title><dc:creator>Peter K.C. Cheng, Kitty K.Y. Wong, Gannon C. Mak, Ann H. Wong, Anita Y.Y. Ng, Salina Y.K. Chow, Ricky K.H. Lam, C.S. Lau, K.C. Ng, Wilina Lim</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.022</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-18</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-18</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Short communications</prism:section><prism:startingPage>182</prism:startingPage><prism:endingPage>185</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005691/abstract?rss=yes"><title>Absence of human bocavirus from deceased fetuses and their mothers</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005691/abstract?rss=yes</link><description>Abstract: Background: The human bocavirus (HBoV), a newly discovered parvovirus, is closely related to the bovine parvovirus and the canine minute virus, which are known to cause adverse pregnancy outcomes. Another human parvovirus, B19, can lead to fetal hydrops, miscarriage and intrauterine fetal death (IUFD).Objectives: To determine the prevalence of HBoV DNA in aborted fetuses and IUFDs. The HBoV serology of the mothers was also studied.Study design: We retrospectively studied all available fetuses (N=535) autopsied during 7/1992–12/1995, and 1/2003–12/2005 in Helsinki, Finland. All available formalin-fixed paraffin-embedded fetal tissues – placenta, heart and liver – of 120 miscarriages, 169 IUFDs, and 246 induced abortions were studied by quantitative PCR. We also measured the HBoV IgM and IgG antibodies in the corresponding maternal sera (N=462) mostly of the first trimester. The IgM-positive sera underwent HBoV PCR.Results: None of the fetal tissues harbored HBoV DNA. A total of 97% (448/462) of the mothers were positive for IgG antibodies to HBoV, while only 0.9% (4/462) exhibited HBoV-specific IgM antibodies without viremia or respiratory symptoms. One IgM-positive mother had an unexplained fetal loss.Conclusions: We did not find HBoV DNA in any of the deceased fetuses. Almost all pregnant women were HBoV-IgG positive.</description><dc:title>Absence of human bocavirus from deceased fetuses and their mothers</dc:title><dc:creator>Anita Riipinen, Elina Väisänen, Anne Lahtinen, Riitta Karikoski, Mika Nuutila, Heljä-Marja Surcel, Helena Taskinen, Klaus Hedman, Maria Söderlund-Venermo</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.028</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Short communications</prism:section><prism:startingPage>186</prism:startingPage><prism:endingPage>188</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS138665320900568X/abstract?rss=yes"><title>Torquetenovirus viremia kinetics after autologous stem cell transplantation are predictable and may serve as a surrogate marker of functional immune reconstitution</title><link>http://www.journalofclinicalvirology.com/article/PIIS138665320900568X/abstract?rss=yes</link><description>Abstract: Background: It is common experience that retreating patients too early after a course of intensive chemotherapy predisposes to opportunistic infections despite apparently normal lymphocyte levels.Objectives: The extent of replication of persistent viruses that cause no obvious disease (and hence need no treatment) might better define when a patient has recovered from functional immune deficiency.Study design: We used real-time polymerase chain reaction to monitor the kinetics of plasma torquetenovirus (TTV) viremia in hematological patients undergoing autologous hematopoietic stem cell transplantation as support to high-dose chemotherapy (HSCT).Results: Independently from underlying hematological disease and therapeutic regimen, TTV viremia increased post-HSCT, and this increase paralleled the increase of circulating CD8+CD57+ T lymphocytes, known to represent an indirect marker of functional immune deficiency. Subsequently, within a matter of months, TTV levels returned to baseline values, at a pace that appeared to be constant over time.Conclusion: Monitoring of TTV viremia represents a unique opportunity to follow functional immune reconstitution in immunosuppressed patients. Also, the size of the TTV viremia increases resulting from immunosuppressive treatments might be of guidance in determining the appropriate time interval before delivery of a next course of therapy.</description><dc:title>Torquetenovirus viremia kinetics after autologous stem cell transplantation are predictable and may serve as a surrogate marker of functional immune reconstitution</dc:title><dc:creator>Daniele Focosi, Fabrizio Maggi, Melania Albani, Lisa Macera, Valentina Ricci, Silvia Gragnani, Serena Di Beo, Massimo Ghimenti, Guido Antonelli, Mauro Bendinelli, Mauro Pistello, Luca Ceccherini-Nelli, Mario Petrini</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.027</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Short communications</prism:section><prism:startingPage>189</prism:startingPage><prism:endingPage>192</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005654/abstract?rss=yes"><title>Reactivation of hepatitis B virus infection with persistently negative HBsAg on three HBsAg assays in a lymphoma patient undergoing chemotherapy</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005654/abstract?rss=yes</link><description>Abstract: In patients with occult hepatitis B virus (HBV) infection, acute exacerbation may occur when they become immunocompromised. Usually, these patients develop hepatitis B surface antigen (HBsAg) seroreversion during the flare. Here we report on a patient with occult HBV infection, who developed HBV exacerbation after chemotherapy for diffuse large B-cell lymphoma. The resurgence of HBV DNA preceded the elevation of liver enzymes for 20 weeks. Atypically, despite high viraemia, serological tests showed persistently negative HBsAg using three different sensitive HBsAg assays (i.e., Architect, Murex and AxSYM). On comparing the amino acid sequence of the index patient with the consensus sequence, five mutations were found at pre-S1, five at pre-S2 and twenty-three mutations at the S region. Six amino acid mutations were located in the ‘a’ determinant, including P120T, K122R, M133T, F134L, D144A and G145A. The mutants K122R, F134L and G145A in our patient have not been tested for their sensitivity to Architect and Murex assays by the previous investigators and might represent the escape mutants to these assays.</description><dc:title>Reactivation of hepatitis B virus infection with persistently negative HBsAg on three HBsAg assays in a lymphoma patient undergoing chemotherapy</dc:title><dc:creator>Wing-I. Cheung, Henry Lik-Yuen Chan, Vincent King-Sun Leung, Chi-Hang Tse, Kitty Fung, Shek-Ying Lin, Ann Wong, Vincent Wai-Sun Wong, Tai-Nin Chau</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.024</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-23</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-23</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Short communications</prism:section><prism:startingPage>193</prism:startingPage><prism:endingPage>195</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005605/abstract?rss=yes"><title>Merkel cell polyomavirus is not detected in mesotheliomas</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005605/abstract?rss=yes</link><description>Abstract: Background: Merkel cell polyomavirus (MCPyV) is the first polyoma virus consistently linked to the etiology of a human cancer. Serological studies indicate that the virus is commonly acquired in childhood, with seroprevalence reaching 50% or higher among young adults. The modes of MCPyV transmission are still unclear, but it has been identified in respiratory tract samples. Given its respiratory tropism, we examined whether MCPyV could be detected in mesothelioma tissue, a malignancy induced in animal models by another polyomavirus, SV40.Objective: To determine if MCPyV DNA can be detected in mesothelioma.Study design: DNA was extracted from 45 fresh-frozen mesothelioma samples. PCR was used to detect and quantify the abundance of MCPyV DNA, and a human control gene, in duplicates of the tissues. DNA from a sequence verified MCC tumor was used as a positive control.Results: The human control gene was detected at high levels in all but three mesothelioma tissues. MCPyV DNA was detected in only one mesothelioma, and the level of viral DNA was very low.Conclusions: These results are inconsistent with the hypothesis that MCPyV is etiologically linked to mesothelioma.</description><dc:title>Merkel cell polyomavirus is not detected in mesotheliomas</dc:title><dc:creator>Kishor Bhatia, Rama Modali, James J. Goedert</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.019</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-14</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-14</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Short communications</prism:section><prism:startingPage>196</prism:startingPage><prism:endingPage>198</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005435/abstract?rss=yes"><title>Swine infuenza (H1N1) pneumonia: Bacterial airway colonization common but fatalities due to bacterial pneumonia remain relatively rare</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005435/abstract?rss=yes</link><description>I read with interest Dr. Kapelusznik's et al., report describing four swine influenza (H1N1) cases with negative rapid influenza diagnostic tests (RIDTs); two purportedly had bacterial community-acquired pneumonia (CAP) which merits comment.</description><dc:title>Swine infuenza (H1N1) pneumonia: Bacterial airway colonization common but fatalities due to bacterial pneumonia remain relatively rare</dc:title><dc:creator>Burke A. Cunha</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.002</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-15</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-15</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>199</prism:startingPage><prism:endingPage>200</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005502/abstract?rss=yes"><title>Human cytomegalovirus in utero transmission: Follow-up of 524 maternal seroconversions</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005502/abstract?rss=yes</link><description>Our group previously described a retrospective study on 141 HCMV seroconversions during pregnancy suggesting an increased risk of transmission during late gestation. Most studies indicate no significant link between age of the pregnancy at infection and infection of the infant, but the literature is limited.</description><dc:title>Human cytomegalovirus in utero transmission: Follow-up of 524 maternal seroconversions</dc:title><dc:creator>Monique Bodéus, Benoît Kabamba-Mukadi, Francis Zech, Corinne Hubinont, Pierre Bernard, Patrick Goubau</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.009</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-14</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-14</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>201</prism:startingPage><prism:endingPage>202</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005666/abstract?rss=yes"><title>Corrigendum to “Varicella-zoster virus CNS disease—Viral load, clinical manifestations and sequels” [J. Clin. Virol. 46 (2009) 249–253]</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005666/abstract?rss=yes</link><description>The authors regret that they made an error in paragraph 3.2. “DNA extraction and real-time PCR detection assay”. The VZV probe sequence was replaced by a CMV probe sequence. The correct probe should be VZV_gB_probe CGCGGTCCCAAGTCCCTGGA.</description><dc:title>Corrigendum to “Varicella-zoster virus CNS disease—Viral load, clinical manifestations and sequels” [J. Clin. Virol. 46 (2009) 249–253]</dc:title><dc:creator>Anna Persson, Tomas Bergström, Magnus Lindh, Lili Namvar, Marie Studahl</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.025</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-28</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-28</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Corrigenda</prism:section><prism:startingPage>203</prism:startingPage><prism:endingPage>203</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209005617/abstract?rss=yes"><title>Corrigendum to “Strengthening the diagnostic capacity to detect Bio Safety Level 3 organisms in unusual respiratory viral outbreaks” [J. Clin. Virol. 45 (2009) 185–190]</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209005617/abstract?rss=yes</link><description>The authors regret that the name of the co-author Charles Boucher was misspelt in the above paper. The correct author list is reproduced above.   The authors would like to apologise for any inconvenience that may have caused to this author and to the readers of the journal.</description><dc:title>Corrigendum to “Strengthening the diagnostic capacity to detect Bio Safety Level 3 organisms in unusual respiratory viral outbreaks” [J. Clin. Virol. 45 (2009) 185–190]</dc:title><dc:creator>Liselotte van Asten, Mariken van der Lubben, Cees van den Wijngaard, Wilfrid van Pelt, Robert Verheij, Andre Jacobi, Pieter Overduin, Adam Meijer, Dirk Luijt, Eric Claas, Mirjam Hermans, Willem Melchers, John Rossen, Rob Schuurman, PetraWolffs, Charles Boucher, Jurjen Schirm, Louis Kroes, Sander Leenders, Joep Galama, Marcel Peeters, Anton van Loon, Ellen Stobberingh, Martin Schutten, Marion Koopmans</dc:creator><dc:identifier>10.1016/j.jcv.2009.11.020</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2009-12-30</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2009-12-30</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section>Corrigenda</prism:section><prism:startingPage>204</prism:startingPage><prism:endingPage>204</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653209006349/abstract?rss=yes"><title>ESCV Membership</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653209006349/abstract?rss=yes</link><description></description><dc:title>ESCV Membership</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1386-6532(09)00634-9</dc:identifier><dc:source>Journal of Clinical Virology 47, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>47</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1386-6532(09)X0019-3</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>I</prism:startingPage><prism:endingPage>II</prism:endingPage></item></rdf:RDF>