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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>49</prism:volume><prism:number>1</prism:number><prism:publicationDate>September 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/PIIS1386653210002957/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210001952/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002349/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002556/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS138665321000257X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002635/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002325/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002623/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002283/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002295/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002581/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002647/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002313/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002301/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002337/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002568/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002660/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002350/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002672/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002982/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journalofclinicalvirology.com/article/PIIS1386653210002994/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002957/abstract?rss=yes"><title>Editorial Board</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002957/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1386-6532(10)00295-7</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>v</prism:startingPage><prism:endingPage>v</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210001952/abstract?rss=yes"><title>Acute retinal necrosis in a monocular patient complicated by acyclovir-induced nephrotoxicity</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210001952/abstract?rss=yes</link><description>A 40 year-old male with history of enucleation of the right eye (OD) during childhood for a “benign tumor” developed sudden photophobia in his left eye (OS). Over the ensuing week, his condition progressed to floaters, blurry vision and injection. The patient was treated with sulfacetamide/prednisolone ophthalmic suspension, followed by fluorometholone. His condition did not improve and he presented to our eye clinic. His exam OS revealed 20/30 acuity, anterior chamber inflammation, 360° peripheral retinal necrosis with hemorrhages, and vitreous haze. A diagnosis of acute retinal necrosis (ARN) was made, intravitreal foscarnet (2.4mg) was given and intravenous (IV) acyclovir (15mg/kg every 8h), topical moxifloxacin, prednisolone and cyclopentolate were started. On the day of admission, his serum creatinine (SCr) was 0.6mg/dL. On the next morning, he received his second dose of IV acyclovir and his SCr was 0.9mg/dL. He received one more dose and prednisone 60mg daily was started. In the morning of the third day his SCr was 3mg/dL. He did not complain of abdominal pain or dysuria and had an otherwise unremarkable physical exam without hypovolemia. During this time, the patient did not receive any concomitant nephrotoxic agents. Renal ultrasound was negative for hydronephrosis or calculi, fractional sodium excretion was 7%, and urine sediment showed no crystals. Acyclovir was discontinued after three doses (total 3g/24h). His SCr peaked at 4.9mg/dL on day 3.What tools are available for diagnosis of ARN?What alternative systemic antiviral drugs are available for therapy?What additional therapeutic modalities should be pursued?</description><dc:title>Acute retinal necrosis in a monocular patient complicated by acyclovir-induced nephrotoxicity</dc:title><dc:creator>Lucio R. Minces, Denise S. Gallagher, Ryan K. Shields</dc:creator><dc:identifier>10.1016/j.jcv.2010.04.016</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-05-31</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-05-31</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Virology Question and Answer Scheme (VIROQAS)</prism:section><prism:startingPage>1</prism:startingPage><prism:endingPage>3</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002349/abstract?rss=yes"><title>Expression profile of Japanese encephalitis virus induced neuroinflammation and its implication in disease severity</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002349/abstract?rss=yes</link><description>Abstract: Background: Host immune response particularly through the induction of proinflammatory cytokines and chemokines in Japanese encephalitis virus infection has not been clearly understood in relation with pathogenicity and disease severity. The newly identified host mediators of pathogenesis could be the future target for diagnostic and therapeutics purpose.Objectives: We investigated the mechanism of JE virus induced pathogenesis in terms of proinflammatory cytokine and chemokine secretion at molecular level in young one-week-old BALB/c mouse after subcutaneous administration of JEV.Study design: Histopathology of brain was done to observe the morphological changes after JEV infection and genes relevant to macrophage activation, chemokine secretion, inflammatory cell infiltration, and blood–brain barrier permeability were examined at their gene and protein expression level for various time points after infection.Results: At 6-day post-infection 100% mortality was observed. At 5-day post-infection, there was a robust expression of proinflammatory cytokines and chemokines with increased number of infiltrating inflammatory cells into the brain. Histopathology data confirms the infiltration of leucocytes and there was a marked upregulation in expression of genes relevant to infiltration. The expression pattern of macrophage receptor CLEC5A/DAP-12 signaling has shown the involvement in this robust neuroinflammation.Conclusions: This is the first report that shows the involvement of monocyte and macrophage receptor CLEC5A in severe inflammatory response in JEV infection of brain. This study at gene expression level provides a hypothesis of neuroinflammation, a new lead in development of appropriate therapeutic, and prophylactics against Japanese encephalitis.</description><dc:title>Expression profile of Japanese encephalitis virus induced neuroinflammation and its implication in disease severity</dc:title><dc:creator>Nimesh Gupta, Vinay Lomash, P.V. Lakshmana Rao</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.009</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-20</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-20</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>4</prism:startingPage><prism:endingPage>10</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002556/abstract?rss=yes"><title>Predictors of spontaneous bleeding in patients with acute febrile syndrome from a dengue endemic area</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002556/abstract?rss=yes</link><description>Abstract: Background: Spontaneous bleeding is a common complication of dengue and is associated with an increased mortality.Objective: To evaluate early clinical manifestations and simple laboratory tests as predictors of spontaneous hemorrhage in patients with forms of acute febrile syndrome (AFS) such as dengue from an endemic area.Study design: A prospective cohort study was performed including 729 non-bleeding AFS patients who were enrolled during the first 4 days of disease. Basal evaluation included anamnesis, physical examination and complete blood cell count. Follow-up was extended at least until the sixth day of disease. Dengue infection was studied with paired serologic tests and viral isolation. Potential predictors of spontaneous bleeding were evaluated with bivariate and multivariate analysis.Results: Incidence of outcome was not significantly different between the dengue group and those with non-dengue AFS. The tourniquet test was not associated with outcome (p=0.38). In a binomial regression model, the following variables were associated with outcome: age between 12 and 45 years (RR=2.22; 95% CI: 1.25–3.94), rash (RR=1.66; 95% CI: 1.25–2.2), vomiting (RR=1.46; 95% CI: 1.16–1.83), temperature &gt;38°C (RR=2.63; 95% CI: 1.6–4.33), leukocyte count &lt;4500/μL (RR=1.87; 95% CI: 1.19–2.96), and platelet count &lt;90.000/μL (RR=1.8; 95% CI: 1.1–2.94). With these variables a risk score was formulated that showed an area under ROC curve of 70.5% (95% CI: 64.9–76.2) to predict spontaneous bleeding. The score was useful for predicting bleeding in both dengue and non-dengue AFS groups.Conclusion: Some variables evaluated in the first days of disease helped to predict the risk of spontaneous bleeding in patients with dengue and non-dengue AFS.</description><dc:title>Predictors of spontaneous bleeding in patients with acute febrile syndrome from a dengue endemic area</dc:title><dc:creator>Fredi Alexander Diaz-Quijano, Luis Angel Villar-Centeno, Ruth Aralí Martinez-Vega</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.011</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-21</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-21</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>11</prism:startingPage><prism:endingPage>15</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS138665321000257X/abstract?rss=yes"><title>Epidemiology of viral respiratory tract infections in a prospective cohort of infants and toddlers attending daycare</title><link>http://www.journalofclinicalvirology.com/article/PIIS138665321000257X/abstract?rss=yes</link><description>Abstract: Background: The epidemiology of respiratory tract infections (RTIs) in a daycare cohort has not been explored using molecular techniques.Objectives: (1) Determine the overall incidence of RTIs in a daycare cohort using real-time reverse transcriptase polymerase chain reaction (RT-PCR). (2) Determine the relative incidence and impact of specific respiratory viruses, and characterize and compare clinical features associated with these pathogens.Study design: In this prospective cohort study conducted from February 2006 to April 2008, nasal swabs were obtained from symptomatic children ages 0–30 months enrolled in fulltime daycare.RT-PCR was performed to detect respiratory syncytial virus (RSV), human metapneumovirus (MPV), influenza (Flu) viruses A and B, parainfluenza (PIV), adenovirus (AdV), human coronaviruses (CoV) and rhinovirus (RhV). Symptom diaries were completed for each illness.Results: We followed 119 children (mean age 10 months; range 2–24 months) for 115 child years. The mean annual incidence of RTI per child was 4.2 the first year and 1.2 the second year of the study. At least 1 virus was identified in 67% RTIs. Co-infections were common (27% RTIs), with RhV, CoV, and AdV the most common co-pathogens. PIV was identified in 12% of RTIs with a high incidence of PIV4. The viruses with the greatest impact on our population were RSV, RhV and AdV.Conclusions: Using molecular techniques, viruses were identified in approximately twice as many RTIs as previously reported in a daycare cohort. Infections with newly identified viruses, such as HMPV and CoV subtypes were less frequent and severe than infections with RSV, AdV and RhV.</description><dc:title>Epidemiology of viral respiratory tract infections in a prospective cohort of infants and toddlers attending daycare</dc:title><dc:creator>Mary P. Fairchok, Emily T. Martin, Susan Chambers, Jane Kuypers, Melinda Behrens, LoRanee E. Braun, Janet A. Englund</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.013</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-23</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-23</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>16</prism:startingPage><prism:endingPage>20</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002635/abstract?rss=yes"><title>Diagnostic accuracy of an allele-specific reverse transcriptase-PCR assay targeting the H275Y oseltamivir resistant mutation in 2009 pandemic influenza A/H1N1 virus</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002635/abstract?rss=yes</link><description>Abstact: Background: Oseltamivir resistant 2009 pandemic influenza A/H1N1 viruses (pH1N1) are emerging and rapid molecular assays identifying these strains are needed for clinical management.Objective: Development and evaluation of an allele-specific, real-time reverse transcriptase-PCR assay (ASPCR) targeting the H275Y oseltamivir resistant mutation in pH1N1 virus.Study design: ASPCR uses two allele-specific forward primers (wild-type and mutant) and a common reverse primer and probe. Wild-type and mutant genotypes were defined by the difference in PCR Ct values (ΔCtmut–wt) between the mutant primer and wild-type primer amplification curves for the same sample. Mixtures of wild-type and mutant genotypes were analyzed to evaluate sensitivity and determine assay cut-off values. ASPCR results were confirmed using an allelic discrimination assay (AD) and pyrosequencing.Results: Mixtures containing 5–95% mutant genotype could be detected. A ΔCtmut–wt≥3.5 identified wild-type genotype (&lt;10% mutant); between 3.5 and −3.5 identified mixed genotypes (10–90% mutant); and ≤−3.5 identified fully mutant genotype (&gt;90% mutant). Among 264 clinical samples, 171 were wild-type, 10 were mixed, and 29 were fully mutant. The 39 samples with mixed or mutant results were from 11 patients. Of 107 samples with sufficient volume tested by ASPCR and AD, 12 were indeterminate by AD due to low viral load, 86 were wild-type by both assays, and 9 were mutant by both assays. Thirteen samples were confirmed by pyrosequencing and one discrepant sample was mixed by ASPCR and fully mutant by pyrosequencing.Conclusions: ASPCR is sensitive, quantitative and specific for H275Y mutation analysis and provides an accurate approach for detecting pH1N1 oseltamivir resistance in clinical samples.</description><dc:title>Diagnostic accuracy of an allele-specific reverse transcriptase-PCR assay targeting the H275Y oseltamivir resistant mutation in 2009 pandemic influenza A/H1N1 virus</dc:title><dc:creator>C. Renaud, J. Kuypers, L. Corey</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.019</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-08-02</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-08-02</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>21</prism:startingPage><prism:endingPage>25</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002325/abstract?rss=yes"><title>No evidence for intrathecal IgG synthesis to Epstein Barr virus nuclear antigen-1 in multiple sclerosis</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002325/abstract?rss=yes</link><description>Abstract: Background: Recent studies suggest an intrathecal IgG response against Epstein Barr virus (EBV) in multiple sclerosis (MS), implicating a pathogenic role for the virus in MS.Objectives: To determine the spectrum of anti-EBV antibodies and B-cell epitopes within EBV nuclear antigen-1 (EBNA-1). Furthermore, to determine whether EBNA-1-specific IgG is produced intrathecally.Study design: Immunoblot analysis was used to study the anti-EBV IgG response in serum and cerebral spinal fluid (CSF) in MS and controls. EBNA-1 B-cell epitopes were identified by immunoscreening of 12 residue long peptides, with 11 residue overlap, spanning EBNA-1. Thirteen peptides containing all immunoreactive regions were constructed and used in paired serum and CSF of MS patients (n=17) and controls (n=18). Subsequently, reactivity to the identified immunodominant peptide was analysed in a large cohort of serum and CSF of MS patients (n=114) and disease controls (n=62).Results: No difference was observed in the overall anti-EBV antibody diversity, but EBNA-1 reactivity was increased in MS patients versus controls for immunoblot and ELISA (p&lt;0.0001). Epitope analysis on EBNA-1 revealed one immunodominant region covering residues 394–451: EBNA-1394–451. Anti-EBNA-1394–451 IgG levels in serum and CSF were significantly higher in MS patients compared to controls. However, normalization for total IgG content of paired serum and CSF samples abrogated this disease association.Conclusions: MS patients have normal overall anti-EBV antibody responses with increased reactivity to EBNA-1394-451. No evidence was found for intrathecal EBNA-1-specific IgG synthesis in MS.</description><dc:title>No evidence for intrathecal IgG synthesis to Epstein Barr virus nuclear antigen-1 in multiple sclerosis</dc:title><dc:creator>Naghmeh Jafari, Gijsbert P. van Nierop, Georges M.G.M. Verjans, Albert D.M.E. Osterhaus, Jaap M. Middeldorp, Rogier Q. Hintzen</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.007</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-20</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-20</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>26</prism:startingPage><prism:endingPage>31</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002623/abstract?rss=yes"><title>Human cytomegalovirus (HCMV) replication kinetics in stem cell transplant recipients following anti-HCMV therapy</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002623/abstract?rss=yes</link><description>Abstract: Background: Cytomegalovirus (HCMV) remains an important infection following stem cell transplantation (SCT) and is managed via pre-emptive therapy. In some patients HCMV loads continue to increase after therapy and they experience multiple episodes of replication.Objectives: To identify the risk factors associated with failure to immediately control HCMV replication after antiviral therapy and for recurrence of replication.Study design: Replication kinetics of human cytomegalovirus (HCMV) were studied a cohort of 153 T-cell depleted allogeneic SCT patients.Results: In 57 patients (31%) who experienced HCMV DNAemia, the mean growth rate of HCMV was 0.35 day−1 equivalent to a doubling time of 2.2 days. In patients requiring anti-HCMV treatment with either ganciclovir or ganciclovir/foscarnet (n=49), HCMV load increased to a peak value of &gt;2 days after initiation of therapy in 21 patients and only the growth rate prior to therapy was a risk factor (Odds ratio=1.4 per 0.1 day−1 increase; p=0.004). In patients where antiviral intervention occurred after peak virus load the decline rate of HCMV load was accelerated 4-fold if the patient was subsequently initiated on anti-HCMV therapy (p=0.02). A subset of patients (38%) experienced a recurrence of their DNAemia at a mean of 20 days after the cessation of their first replication episode and this was only associated with receiving stem cells from a seronegative donor (Odds ratio=6.59; p&lt;0.001).Conclusions: The kinetics of response to therapy is closely associated with HCMV replication kinetics prior to therapy while recurrence of replication is associated with HCMV serostatus of the donor.</description><dc:title>Human cytomegalovirus (HCMV) replication kinetics in stem cell transplant recipients following anti-HCMV therapy</dc:title><dc:creator>Hubertus C.E. Buyck, Paul D. Griffiths, Vincent C. Emery</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.018</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-28</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-28</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>32</prism:startingPage><prism:endingPage>36</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002283/abstract?rss=yes"><title>Development of real-time PCR assay for specific detection of cowpox virus</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002283/abstract?rss=yes</link><description>Abstract: Background: The number of recorded human cowpox cases are recently increasing. The symptoms caused by cowpox virus (CPXV) in a number of human cases are close to the symptoms characteristic of the orthopoxviral human infections caused by monkeypox or smallpox (variola) viruses. Any rapid and reliable real-time PCR method for distinguishing cowpox from smallpox and monkeypox is yet absent.Objectives: The aim of this study was to develop a quick and reliable real-time TaqMan PCR assay for specific detection of cowpox virus and to determine the sensitivity and specificity of this method.Study design: Based on aligned nucleotide sequences of orthopoxviruses, we found a virus-specific region in the CPXV genome and selected the oligonucleotide primers and hybridization probe within this region. The specificity of the developed method was tested using a panel of various orthopoxvirus (OPV) DNAs. The sensitivity was determined using the recombinant plasmid carrying a fragment of CPXV DNA and genomic DNA of the CPXV strain GRI-90.Results: The analytical specificity of this method was determined using DNAs of 17 strains of four OPV species pathogenic for humans and amounted to 100%. The method allows 6 copies of plasmid DNA and 20 copies of CPXV DNA in the reaction mixture to be detected.Conclusion: A quick and reliable TaqMan PCR assay providing for a highly sensitive and specific detection of CPXV DNA was developed.</description><dc:title>Development of real-time PCR assay for specific detection of cowpox virus</dc:title><dc:creator>Elena V. Gavrilova, Dmitrii N. Shcherbakov, Rinat A. Maksyutov, Sergei N. Shchelkunov</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.003</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>37</prism:startingPage><prism:endingPage>40</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002295/abstract?rss=yes"><title>Improved HIV-1 RNA quantitation by COBAS® AmpliPrep/COBAS® TaqMan® HIV-1 Test, v2.0 using a novel dual-target approach</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002295/abstract?rss=yes</link><description>Abstract: Background: HIV-1 RNA viral load is a key parameter for reliable treatment monitoring of HIV-1 infection. Accurate HIV-1 RNA quantitation can be impaired by primer and probe sequence polymorphisms as a result of tremendous genetic diversity and ongoing evolution of HIV-1. A novel dual HIV-1 target amplification approach was realized in the quantitative COBAS® AmpliPrep/COBAS® TaqMan® HIV-1 Test, v2.0 (HIV-1 TaqMan® test v2.0) to cope with the high genetic diversity of the virus.Objectives and study design: The performance of the new assay was evaluated for sensitivity, dynamic range, precision, subtype inclusivity, diagnostic and analytical specificity, interfering substances, and correlation with the COBAS® AmpliPrep/COBAS® TaqMan® HIV-1 (HIV-1 TaqMan® test v1.0) predecessor test in patients specimens.Results: The new assay demonstrated a sensitivity of 20copies/mL, a linear measuring range of 20–10,000,000copies/mL, with a lower limit of quantitation of 20copies/mL. HIV-1 Group M subtypes and HIV-1 Group O were quantified within ±0.3log10 of the assigned titers. Specificity was 100% in 660 tested specimens, no cross reactivity was found for 15 pathogens nor any interference for endogenous substances or 29 drugs. Good comparability with the predecessor assay was demonstrated in 82 positive patient samples. In selected clinical samples 35/66 specimens were found underquantitated in the predecessor assay; all were quantitated correctly in the new assay.Conclusions: The dual-target approach for the HIV-1 TaqMan® test v2.0 enables superior HIV-1 Group M subtype coverage including HIV-1 Group O detection. Correct quantitation of specimens underquantitated in the HIV-1 TaqMan® test v1.0 test was demonstrated.</description><dc:title>Improved HIV-1 RNA quantitation by COBAS® AmpliPrep/COBAS® TaqMan® HIV-1 Test, v2.0 using a novel dual-target approach</dc:title><dc:creator>Dorothea Sizmann, Joachim Glaubitz, Christian O. Simon, Sebastian Goedel, Philippe Buergisser, Daniel Drogan, Martin Hesse, Michael Kröh, Pascale Simmler, Manuela Dewald, Marion Gilsdorf, Marion Fuerst, Ralph Ineichen, Anette Kirn, Paul Pasche, Zhijun Wang, Sabrina Weisshaar, Karen Young, Gerd Haberhausen, Reiner Babiel</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.004</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-16</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-16</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>41</prism:startingPage><prism:endingPage>46</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002581/abstract?rss=yes"><title>Transmission dynamics of rabies in China over the last 40 years: 1969–2009</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002581/abstract?rss=yes</link><description>Abstract: Background: Rabies is a serious reemerging zoonosis in China. The molecular evolution and transmission patterns of rabies virus inferred from historical data can provide guidelines for better disease control and prevention in the future.Objectives: To investigate the epidemiology and evolutionary dynamics of the rabies virus in China.Study design: The molecular evolution of 132 viral glycoprotein gene sequences of Chinese rabies viruses collected in 17 provinces and 3 municipalities between 1969 and 2009 was analyzed.Results: Phylogenetic analysis revealed that Chinese rabies viruses are subdivided into 6 lineages (A–F) within Lyssavirus genotype 1. Lineage A represents the widely dispersed cosmopolitan lineage while lineage B is closely related to Arctic-like rabies viruses. The remaining lineages (C–F) are typical of those circulating across much of Southeast Asia. The evolutionary rate for Chinese rabies virus was 1.532×10−4 substitutions per site per year, and the corresponding common ancestor was in about 1115.Conclusions: The phylogeographic structure demonstrated Chinese rabies viruses have been transmitted intra-provincially and extra-provincially due to human-related activities.</description><dc:title>Transmission dynamics of rabies in China over the last 40 years: 1969–2009</dc:title><dc:creator>Shengli Meng, Gelin Xu, Xianfu Wu, Yongliang Lei, Jiaxin Yan, Susan A. Nadin-Davis, Hong Liu, Jie Wu, Dingming Wang, Guanmu Dong, Xiaoming Yang, Charles E. Rupprecht</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.014</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-23</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-23</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>47</prism:startingPage><prism:endingPage>52</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002647/abstract?rss=yes"><title>Successful outcome of kidney transplantation from a HBV-DNA positive donor into recipients with cleared HBV-infection using a pre-emptive therapy approach</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002647/abstract?rss=yes</link><description>Abstract: Background: Donor-derived transmission of hepatitis B virus (HBV) may cause serious complications after transplantation. To date, transplantation from HBV-infected donors to HBV-infected recipients seems feasible, although this is recommended with prophylaxis with specific drugs and antibodies only, whereas pre-emptive strategies are rarely used.Objectives: Here, we assessed the success of transplantation of kidneys from a chronically HBV-infected deceased donor (HBs-antigen positive, anti-HBc positive, HBV-DNA positive) to two recipients with cleared HBV-infection (HBs-antigen negative, anti-HBc positive, anti-HBs &gt;100IU/l) where risk-assessment was performed using a pre-emptive approach in the absence of prophylaxis.Study design: Pre-emptive monitoring included assessment for evidence of infection by analysis of liver enzymes, viral load, and humoral and cellular immunity against HBV and CMV.Results: In line with undetectable HBV-load, HBc-specific T-cell frequencies remained stable (mean 0.46±0.10% and 0.06±0.03%), whereas CMV-specific T-cell frequencies in one patient showed dynamic changes that coincided with CMV-viremia. Likewise, HBV-specific antibody titres were stable. Liver enzymes demonstrated absence of liver-cell injury and renal function was good (creatinine 1.8 and 0.8mg/dl at last follow-up after 39 and 38 months, respectively).Conclusions: When combined with careful HBV-monitoring, kidneys from HBV-infected donors may be transplanted into HBV-immune recipients without the need for specific prophylaxis.</description><dc:title>Successful outcome of kidney transplantation from a HBV-DNA positive donor into recipients with cleared HBV-infection using a pre-emptive therapy approach</dc:title><dc:creator>Janine Mohrbach, Martin W.W. Janssen, Gunnar H. Heine, Barbara C. Gärtner, Danilo Fliser, Martina Sester, Urban Sester</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.020</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-26</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-26</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Full length articles</prism:section><prism:startingPage>53</prism:startingPage><prism:endingPage>57</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002313/abstract?rss=yes"><title>Direct immunofluorescence assay compared to cell culture for the diagnosis of mucocutaneous herpes simplex virus infections in children</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002313/abstract?rss=yes</link><description>Abstract: Background: Direct immunofluorescence assay (DFA) is commonly used for the rapid identification of herpes simplex virus (HSV) infection in mucocutaneous lesions, yet little is known about its diagnostic accuracy.Objective: To determine the diagnostic yield and accuracy of HSV DFA for the diagnosis of mucocutaneous HSV infection in pediatric patients.Study design: Retrospective cross-sectional study of all patients who underwent HSV DFA testing by the Texas Children's Hospital Diagnostic Virology between January 1, 1995 and December 31, 2005. HSV DFA sensitivity, specificity, positive likelihood ratio (LRs), and negative LRs were estimated using viral culture as the reference standard.Results: 659 specimens were submitted for HSV DFA with concurrent viral cultures. Viral cultures were positive for HSV type 1 in 158 (24%) and HSV type 2 in 2 (0.3%). There were 433 different patients with a median age of 8.6 years. Types of lesions were as follows: 50% ulcerative, 26% vesicular, 8% erythema or purpura, 5% pustular, and 11% missing. Of the 659 specimens submitted for HSV DFA, 160 (24%) were inconclusive due to inadequate cells. Of the 499 adequate specimens, overall HSV DFA test accuracy was: sensitivity 61%, specificity 99%, LR positive 40, and LR negative 0.39.Conclusions: A quarter of specimens submitted for HSV DFA testing are not adequate for DFA testing. When HSV DFA can be performed, it is specific, but not sensitive, for the identification of mucocutaneous HSV infection in children.</description><dc:title>Direct immunofluorescence assay compared to cell culture for the diagnosis of mucocutaneous herpes simplex virus infections in children</dc:title><dc:creator>A. Chantal Caviness, Lindsay L. Oelze, Ulas E. Saz, Jewel M. Greer, Gail J. Demmler-Harrison</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.006</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-12</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-12</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Short communications</prism:section><prism:startingPage>58</prism:startingPage><prism:endingPage>60</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002301/abstract?rss=yes"><title>Evaluation of core and NS4B synthetic peptide-based immunoassays for the detection of hepatitis C virus antibodies in clinical samples from Cameroon, Central Africa</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002301/abstract?rss=yes</link><description>Abstract: Background: According to previous data, the antibodies produced during natural hepatitis C virus (HCV) infection frequently recognize amino acids 10–43 in the core protein and 1689–1740 or 1921–1940 in the non-structural 4B (NS4B) protein. The reactivity of these peptides with the corresponding antibodies has mainly been evaluated using serum samples from Western countries where HCV genotype 1 (HCV-1) is predominant, and no information is available concerning samples from sub-Saharan countries where high HCV variability has been reported.Objective of this study: To evaluate the performance of HCV core and NS4B peptide-based immunoassays in the serodiagnosis of HCV infection in Cameroon subjects.Study design: Three core and four NS4B-based synthetic peptides derived from HCV genotypes 1b and 2a were designed and tested against a panel of 151 serum samples from Cameroon (40 positive for HCV-1, 32 for HCV-2, 39 HCV-4, and 40 HCV-negative).Results: The three core peptides all demonstrated strong immunoreactivity, regardless of the HCV genotype from which they were derived, with greater than 90% and 92% sensitivity and specificity. In contrast, the NS4B-derived peptides exhibited lower sensitivities (24.3–65.8% depending on the HCV genotype) but higher specificities (100% for all four peptides tested).Conclusions: Our findings indicate that an HCV core peptide could be used for the diagnosis of chronic HCV infection. Among the NS4B peptides tested, a chimeric NS4B peptide encompassing both N- and C-terminal portions of the NS4B protein gave a much better performance than the two component N- and C-terminal peptides used individually.</description><dc:title>Evaluation of core and NS4B synthetic peptide-based immunoassays for the detection of hepatitis C virus antibodies in clinical samples from Cameroon, Central Africa</dc:title><dc:creator>Richard Njouom, Eric Nerrienet, Agata Budkowska, Patrick Maillard, Dominique Rousset, Olga Kalinina, Penelope Mavromara, the HCV Collaborative Team of the International Pasteur Network</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.005</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-12</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-12</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Short communications</prism:section><prism:startingPage>61</prism:startingPage><prism:endingPage>64</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002337/abstract?rss=yes"><title>Acute hepatitis C infection with evidence of heterosexual transmission</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002337/abstract?rss=yes</link><description>Abstract: A 62-year-old woman acquired acute hepatitis C virus (HCV) infection after heterosexual contact with a known HCV positive former injecting drug user. There were no known sexual or other risk factors for HCV acquisition. Phylogenetic analysis confirmed the case and index were infected with identical genotype 3a strains, consistent with heterosexual transmission in the absence of specific risk factors.</description><dc:title>Acute hepatitis C infection with evidence of heterosexual transmission</dc:title><dc:creator>Oanh Nguyen, Vicky Sheppeard, Mark W. Douglas, Elise Tu, William Rawlinson</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.008</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-28</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-28</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Short communications</prism:section><prism:startingPage>65</prism:startingPage><prism:endingPage>68</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002568/abstract?rss=yes"><title>Evaluation of new hemagglutinin-based rapid antigen test for influenza A pandemic (H1N1) 2009</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002568/abstract?rss=yes</link><description>Abstract: Background: A new rapid antigen test (RAT), based on hemagglutinin, was developed for the improvement of influenza A pandemic (H1N1) 2009 detection.Objective: To evaluate the performance of the new RAT for the diagnosis of influenza A pandemic (H1N1) 2009.Study design: The new RAT included 2009 H1N1 hemagglutinin-based band and influenza A and influenza B nucleoprotein-based bands. During the period from November 24, 2009 to December 14, 2009, 948 patients underwent the new RAT and real-time reverse transcriptase polymerase chain reaction (rRT-PCR) at the same time. The result of the new RAT was compared with that of rRT-PCR, and the results of hemagglutinin-based and nucleoprotein-based antigen tests were compared.Result: Among the 260 patients confirmed by rRT-PCR, 153 (58.8%) were positive in the nucleoprotein-based antigen test, and 182 (70.0%) were positive in the hemagglutinin-based antigen test. These results show that the new hemagglutinin-based antigen test was more sensitive than the nucleoprotein-based antigen test for the detection of influenza A pandemic (H1N1) 2009 (p&lt;0.001, the McNemar test).Conclusion: The new hemagglutinin-based antigen test improved the sensitivity of diagnosis for influenza A pandemic (H1N1) 2009 and it might be helpful for the diagnosis of influenza A pandemic (H1N1) 2009.</description><dc:title>Evaluation of new hemagglutinin-based rapid antigen test for influenza A pandemic (H1N1) 2009</dc:title><dc:creator>Young Keun Kim, Young Uh, Jin-Kyong Chun, Changsoo Kim, Hyo Youl Kim</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.012</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-22</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-22</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Short communications</prism:section><prism:startingPage>69</prism:startingPage><prism:endingPage>72</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002660/abstract?rss=yes"><title>Comparative evaluation of Taqman real-time PCR and semi-nested VP1 PCR for detection of enteroviruses in clinical specimens</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002660/abstract?rss=yes</link><description>Abstract: Background: Molecular diagnostic tests to detect enterovirus in clinical specimens usually target highly conserved sites in the 5′-non-translated region, allowing detection of all members of the genus. The sequences in the 5′-NTR do not correlate with serotype, but PCR and sequencing of the VP1 region can be used for typing; this system has largely replaced traditional antigenic typing.Objective: To investigate the relative performance of two common enterovirus assays.Study design: We compared the relative sensitivities of Taqman® real-time RT-PCR (rRT-PCR) and a VP1 semi-nested PCR (RT-snPCR) assay in which sequencing the VP1 amplicon also provides typing information.Results: There was 89% concordance between the two methods among the 371 clinical specimens tested (74 positive in both assays and 257 negative in both assays). Twenty-seven rRT-PCR-negative/VP1-positive specimens were confirmed positive by sequencing; 13 specimens were rRT-PCR-positive/VP1-negative.Conclusions: The results suggest that either assay can produce satisfactory results, but that using both assays in parallel should provide the highest sensitivity for clinical diagnostic testing.</description><dc:title>Comparative evaluation of Taqman real-time PCR and semi-nested VP1 PCR for detection of enteroviruses in clinical specimens</dc:title><dc:creator>M. Steven Oberste, Silvia Peñaranda, Shannon L. Rogers, Elizabeth Henderson, W. Allan Nix</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.022</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-28</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-28</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Short communications</prism:section><prism:startingPage>73</prism:startingPage><prism:endingPage>74</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002350/abstract?rss=yes"><title>Epidemiological and clinical characterization of norovirus infections among hospitalized children in Baranya County, Hungary</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002350/abstract?rss=yes</link><description>Norovirus (NV) is recognized as an important cause of food and water borne gastroenteritis worldwide. In the community-based studies the prevalence of NV infection has been reported to be 1–22%, while many outbreaks of NV were also reported. The aim of this study was to emphasize the importance of NV infections among children hospitalized with acute gastroenteritis based on the epidemiological and clinical data. The present report is an adjunct to the study in which we carried out analyses on viral gastroenteritis using the same sample set.</description><dc:title>Epidemiological and clinical characterization of norovirus infections among hospitalized children in Baranya County, Hungary</dc:title><dc:creator>Ferenc Jakab, Viktória Németh, Miklós Oldal, Levente Varga, Zoltán Nyul, Miklós Oldal, Douglas K. Mitchell, David O. Matson, Miklós Oldal, Gy. Szűcs, Miklós Oldal</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.010</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-20</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-20</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>75</prism:startingPage><prism:endingPage>76</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002672/abstract?rss=yes"><title>Apropos “Evaluation of a rapid, point-of-care device for the diagnosis of hepatitis C infection”</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002672/abstract?rss=yes</link><description>We laud research on OraQuick®, the rapid hepatitis C (HCV) point-of-care diagnostic device for use at clinics, physician offices and community out reach centers. To ensure global OraQuick® acceptability, the stability of the test while in use in the field, cost per test and competing alternate options require immediate consideration.</description><dc:title>Apropos “Evaluation of a rapid, point-of-care device for the diagnosis of hepatitis C infection”</dc:title><dc:creator>Subhash C. Arya, Nirmala Agarwal</dc:creator><dc:identifier>10.1016/j.jcv.2010.06.023</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-07-28</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-07-28</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>77</prism:startingPage><prism:endingPage>77</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002982/abstract?rss=yes"><title>ESCV Membership</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002982/abstract?rss=yes</link><description></description><dc:title>ESCV Membership</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1386-6532(10)00298-2</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>I</prism:startingPage><prism:endingPage>II</prism:endingPage></item><item rdf:about="http://www.journalofclinicalvirology.com/article/PIIS1386653210002994/abstract?rss=yes"><title>ESCV Meeting Calendar</title><link>http://www.journalofclinicalvirology.com/article/PIIS1386653210002994/abstract?rss=yes</link><description></description><dc:title>ESCV Meeting Calendar</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1386-6532(10)00299-4</dc:identifier><dc:source>Journal of Clinical Virology 49, 1 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Journal of Clinical Virology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>49</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1386-6532(10)X0009-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>III</prism:startingPage><prism:endingPage>IV</prism:endingPage></item></rdf:RDF>