33 research outputs found

    Epidemiological and Clinical Features of Severe Fever with Thrombocytopenia Syndrome in Japan, 2013–2014 - Fig 2

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    <p>Serial concentrations of aspartate aminotransferase (A) and lactate dehydrogenase (B) in 15 fatal SFTS cases during hospitalization. The number in parenthesis of each patient indicates the days after disease onset when each patient died. A single result was available for the patient no.1. The normal ranges for each parameter are 10–35 IU/L for AST, and 120–220 IU/L for serum LDH.</p

    Laboratory findings for SFTS cases.

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    <p>White blood cells (A), platelets (B), aspartate aminotransferase concentration (C), and lactate dehydrogenase concentration (D) in nonfatal and fatal cases at the time of admission and during hospitalization. Laboratory data are shown as the median and interquartile range between the first and third quartiles. Solid lines indicate nonfatal cases and dotted lines indicate fatal cases. The numbers of nonfatal and fatal cases are indicated for each onset day below the graph. The normal ranges for each parameter are 3,500–9,000/μL for WBC count, 15–35 × 10<sup>4/</sup>μL for platelet count, 10–35 IU/L for AST, and 120–220 IU/L for serum LDH. * p < 0.05 between nonfatal and fatal cases.</p

    Growth kinetics of RVΔP-LCMV/GPC and RVΔP in BHK-P cells.

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    <p>BHK-P cells were inoculated with RVΔP-LCMV/GPC or RVΔP at an MOI of 0.01. Culture supernatants were harvested at 1, 3, 5, and 7 days post inoculation, and virus titers were determined using BHK-P cells. The data were expressed as mean ± SE of 4 independent experiments. Asterisks indicate a significant difference (p < 0.05).</p

    Confirmation of RV-N and LCMV-GP expression.

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    <p>BHK-P cells were inoculated with RVΔP-LCMV/GPC (A–C) or RVΔP (D–F) at an MOI of 0.1 and incubated at 33°C for 48 h. Cells were stained with anti-RV N mAb or the anti-LCMV-GP1 mAb. Original magnification, 400×. (G–I) RV-N and the LCMV-GPC were detected in Neuro-2a cells inoculated with RVΔP-LCMV/GPC at an MOI of 8 at 48 h post inoculation). Original magnification, 200×. (J) GPC (70 KDa) and GP1 (40 KDa) proteins were detected in BHK-P cells infected with RVΔP-LCMV/GPC by western blot using the anti-LCMV-GP1 mAb. (K–L) The cultured medium (Sup) of cells infected with RVΔP-LCMV/GPC or RVΔP were PEG precipitated (PEG ppt) and purified (Purified) by ultracentrifugation and stained with the anti LCMV-GP1 Mab (K) or the anti-RV G mAb (L). The lysates of mock-inoculated Vero cells and LCMV-WE -inoculated Vero cells were used as negative and positive controls, respectively (K). Lysates of mock-inoculated Neuro-2a cells and RV HEP-Flury strain-infected Neuro-2a cells were used as negative and positive controls, respectively (L).</p

    Survival curves and NAb titers in mice infected with LCMV-WE with or without CD8+ T cell depletion.

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    <p>(A) RVΔP-LCMV/GPC inoculation, challenge, and blood collection schedules in C57BL/6 mice. Mice were inoculated with RVΔP-LCMV/GPC twice at 3-week intervals. Mice were injected with anti-CD8+ T cell antibody (n = 6) or Isotype control (n = 6) 4 days and 7 days after the last RVΔP-LCMV/GPC inoculation. Seven days after the last inoculation, mice were intracranially infected with 10 PFU of LCMV-WE. Mouse serum was collected 1 day before the first RV inoculation (Pre) and second RV inoculation (1st), and the serum of the surviving mice was collected on the last day of the 3-week observation (Post). (B) The survival curve of mice injected with CD8+ T cell antibody or isotype control. The titers of anti-LCMV (C) and anti-RV (D) NAb in mice with and without CD8+ T-cell depletion.</p
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