10 research outputs found

    Sequencing results and schematic representation of the EKV-1 and -2 genome organization.

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    <p>(<b>A</b>) Overview of the data generated for each novel rhabdovirus. (<b>B</b>) A schematic showing the assembled genomes, consisting of the following genes: <i>nucleoprotein</i> (N), <i>phosphoprotein</i> (P), <i>matrix</i> (M), <i>U1</i>/<i>U2</i>/<i>U3</i> (uncharacterized accessory proteins), <i>glycoprotein</i> (G), and <i>polymerase</i> (L). We indicate in orange (EKV-1) and blue (EKV-2) segments of the viral genomes that could not be assembled from Illumina reads and instead Sanger sequenced. (<b>C</b>) Coverage plots of the final viral genomes.</p

    Examples of rhabdoviruses reported in Africa.

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    <p>A map depicting examples of rhabdoviruses isolated in sub-Saharan Africa. This map does not depict the current distribution of rhabdoviruses in Sub-Saharan Africa, nor is it meant as a comprehensive listing of all rhabdoviruses isolated in Africa; rather its purpose is to illustrate that many rhabdoviruses have been discovered throughout Africa over the past half-century. Country refers to the sample’s country of origin. Abbreviations: CAR, Central African Republic; DRC, Democratic Republic of Congo.</p

    Suspected cases of LF evaluated at the KGH Lassa Laboratory and numbers of patients admitted to the KGH Lassa Ward, 2008–12.

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    <p>Non-admitted patients include those where only blood samples were submitted for screening from referral health-posts, patients dying en route to the hospital (DOA = dead on arrival), and patients not meeting the LF suspected case criteria (<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002748#pntd-0002748-t001" target="_blank">Table 1</a>). Characteristics of study patients are compiled in <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002748#pntd.0002748.s002" target="_blank">Table S1</a>.</p

    Age distribution of cases presenting to the KGH Lassa Ward, 2008–12.

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    <p>Panel A: Age distributions of patients presenting while antigenemic (Ag+/IgM±). Panel B: Age distributions of nonantigenemic patients presenting with serum anti-LASV IgM (Ag−/IgM+). Panel C: Age distributions of nonantigenemic patients presenting without anti-LASV IgM seropositivity (Ag−/IgM−). In Panels A–C yellow portion of bars represent patients who were discharged and black portion of bars represent patients who died. Panel D: Age demographic for the population of Sierra Leone (2010 estimate). Among patients who died, the age distributions differed significantly between the Ag+/IgM± and Ag−/IgM− groups (p = .005). Distributional comparisons were carried out using the Kolmogorov-Smirnov technique (<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002748#pntd.0002748.s006" target="_blank">Table S5</a>).</p

    Case fatality rates for suspected LF cases by ribavirin treatment status and serostatus.

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    <p>The presence of LASV Ag in serum of patients with observed survival outcomes and verified treatment status was assessed by recombinant Ag− and IgM-capture ELISA. Statistical significance for within and between group comparisons was determined using a multivariate logistic regression model (<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002748#pntd.0002748.s010" target="_blank">Table S9</a>). NS = not significant.</p

    CFRs in suspected LF cases presenting to the KGH Lassa Ward by serostatus, 2008–12.

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    <p>Panel A: CFR by serostatus. The presence of LASV Ag and anti-LASV IgM in serum of patients with verifiable outcomes was assessed by recombinant Ag− and IgM− capture ELISA, respectively. Panel B: Alternative calculation of CFRs. Ag+/IgM± plus Ag−/IgM+ compared to Ag−/IgM−. Statistical significance was determined using a logistic regression model predicting CFR (<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002748#pntd.0002748.s004" target="_blank">Table S3</a>). NS = not significant.</p

    Geographic distribution of patients presenting to the KGH with LASV antigenemia and anti-LASV IgM serpositivity, 2008–12.

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    <p>Confirmed cases of LF as assessed by LASV Ag in serum or cases anti-LASV IgM are shown by year of presentation, district of residence and frequency of cases. Panel A: Patients presenting in 2008–9. Panel B: Patients presenting in 2010. Panel C: Patients presenting in 2011. Panel D: Patients presenting in 2012.</p

    Monthly distribution of suspected LF cases presenting to the KGH Lassa Ward by serostatus, 2008–2012.

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    <p>Panel A: antigenemic Lassa fever cases (Ag+/IgM±). Panel B: Patients with serum anti-LASV IgM (Ag−/IgM+). Panel C: Patients with no Lassa virus seropositivity (Ag−/IgM−). The monthly frequency distributions differed between each of the serostatus group comparisons as assessed using a Poisson regression model (p<.001 for all serostatus comparisons; data not shown).</p

    Gender and self-reported pregnancy status of suspected Lassa fever cases presenting to the KGH Lassa Ward, 2008–2012.

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    <p>Panel A: Frequency of suspected Lassa fever cases by gender and serostatus. Panel B: Cases fatality rates by gender and serostatus. Panel C: Percentage of female patients of childbearing age with self-reported pregnancy status by serostatus. Panel D: Case fatality rates in female patients with self-reported pregnancy status Pregnancies are self-reported and therefore likely underestimated as pregnancy tests were not routinely available. Logistic regression was used for group comparisons (<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002748#pntd.0002748.s007" target="_blank">Tables S6</a> and <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002748#pntd.0002748.s008" target="_blank">S7</a>). NS = not significant.</p
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