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Estimation of level of agreement for anti‐HCV assays and with HCV PCR
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Estimation of level of agreement for anti‐HCV assays and with HCV PCR
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Time of addition kinetics <t>with</t> <t>BAY</t> 81-8781 and assessment of emergence of resistance. A549 cells were infected with A/Mallard/Bavaria/1/2006 (MB1) (MOI: 0.001). Twenty-four hours after infection cells were treated with five different concentrations of BAY 81-8781 ranging from 0.001 to 10 mM for either 30 min (A) , 1 h (B) , 2 h (C) or 4 h (D) . Either 6 h, 12 h, 18 h, or 24 h after infection supernatant was harvested. Virus titer was determined as indicated in the “Materials and Materials” section. Virus titer differed in controls depending on the time the supernatant was harvested after start of treatment. Therefore, only virus titer in percent compared to control is given in this figure, which allows the comparison of all graphs. (E) BAY 81-8781-treatment does not lead to emergence of resistant virus variant upon multiple passaging in cell culture. A549 lung epithelial cells were infected with IAV A/FPV/Bratislava/79 (H7N7) (FPV, fowl plague virus) at a MOI = 0.01 and incubated for 24 h with either BAY 81-8781 (5 mM) or <t>oseltamivir</t> (2 μM). Cell culture supernatants were removed and used to determine viral titers in plaque assays on MDCK cells. Supernatants were adjusted in titers and used for a second infection round in presence or absence of the inhibitors. This procedure was repeated until passage eight. Virus titers are shown relative to titers of untreated control cells (black bars) that were normalized to 100%. p -values of < 0.05 are referred to ∗ .
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Time of addition kinetics <t>with</t> <t>BAY</t> 81-8781 and assessment of emergence of resistance. A549 cells were infected with A/Mallard/Bavaria/1/2006 (MB1) (MOI: 0.001). Twenty-four hours after infection cells were treated with five different concentrations of BAY 81-8781 ranging from 0.001 to 10 mM for either 30 min (A) , 1 h (B) , 2 h (C) or 4 h (D) . Either 6 h, 12 h, 18 h, or 24 h after infection supernatant was harvested. Virus titer was determined as indicated in the “Materials and Materials” section. Virus titer differed in controls depending on the time the supernatant was harvested after start of treatment. Therefore, only virus titer in percent compared to control is given in this figure, which allows the comparison of all graphs. (E) BAY 81-8781-treatment does not lead to emergence of resistant virus variant upon multiple passaging in cell culture. A549 lung epithelial cells were infected with IAV A/FPV/Bratislava/79 (H7N7) (FPV, fowl plague virus) at a MOI = 0.01 and incubated for 24 h with either BAY 81-8781 (5 mM) or <t>oseltamivir</t> (2 μM). Cell culture supernatants were removed and used to determine viral titers in plaque assays on MDCK cells. Supernatants were adjusted in titers and used for a second infection round in presence or absence of the inhibitors. This procedure was repeated until passage eight. Virus titers are shown relative to titers of untreated control cells (black bars) that were normalized to 100%. p -values of < 0.05 are referred to ∗ .
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Time of addition kinetics <t>with</t> <t>BAY</t> 81-8781 and assessment of emergence of resistance. A549 cells were infected with A/Mallard/Bavaria/1/2006 (MB1) (MOI: 0.001). Twenty-four hours after infection cells were treated with five different concentrations of BAY 81-8781 ranging from 0.001 to 10 mM for either 30 min (A) , 1 h (B) , 2 h (C) or 4 h (D) . Either 6 h, 12 h, 18 h, or 24 h after infection supernatant was harvested. Virus titer was determined as indicated in the “Materials and Materials” section. Virus titer differed in controls depending on the time the supernatant was harvested after start of treatment. Therefore, only virus titer in percent compared to control is given in this figure, which allows the comparison of all graphs. (E) BAY 81-8781-treatment does not lead to emergence of resistant virus variant upon multiple passaging in cell culture. A549 lung epithelial cells were infected with IAV A/FPV/Bratislava/79 (H7N7) (FPV, fowl plague virus) at a MOI = 0.01 and incubated for 24 h with either BAY 81-8781 (5 mM) or <t>oseltamivir</t> (2 μM). Cell culture supernatants were removed and used to determine viral titers in plaque assays on MDCK cells. Supernatants were adjusted in titers and used for a second infection round in presence or absence of the inhibitors. This procedure was repeated until passage eight. Virus titers are shown relative to titers of untreated control cells (black bars) that were normalized to 100%. p -values of < 0.05 are referred to ∗ .
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Estimation of level of agreement for anti‐HCV assays and with HCV PCR

Journal: Journal of Clinical Laboratory Analysis

Article Title: Diagnostic reliability of Architect anti‐HCV assay: Experience of a tertiary care hospital in India

doi: 10.1002/jcla.22245

Figure Lengend Snippet: Estimation of level of agreement for anti‐HCV assays and with HCV PCR

Article Snippet: The level of agreement as assessed by kappa is shown in Table . table ft1 table-wrap mode="anchored" t5 Table 1 caption a7 Level of agreement (κ‐value) Anti‐ HCV antibody assays (n=1000) Architect anti‐HCV a vs HCV TRI‐DOT b .16 Architect anti‐HCV vs ORTHO HCV c .26 ORTHO HCV vs HCV TRI‐DOT .68 Anti‐HCV antibody assays vs HCV PCR d (n=500) Architect anti‐HCV .27 ORTHO HCV .62 HCV TRI‐DOT .81 Open in a separate window a ARCHITECT anti‐HCV (Abbott, USA) works on the principle of chemiluminescent microparticle immunoassay (CMIA). b HCV TRI‐DOT (J. Mitra, New Delhi, India)—Rapid visual test works on the principle of immunofiltration. c ORTHO HCV 3.0 ELISA Test (Ortho Clinical Diagnostics, Raritan, NJ, USA) works on the principle of enzyme immunoassay. d Abbott real‐time HCV‐PCR (Abbott Molecular Inc., Des Plaines, IL, USA).

Techniques:

Time of addition kinetics with BAY 81-8781 and assessment of emergence of resistance. A549 cells were infected with A/Mallard/Bavaria/1/2006 (MB1) (MOI: 0.001). Twenty-four hours after infection cells were treated with five different concentrations of BAY 81-8781 ranging from 0.001 to 10 mM for either 30 min (A) , 1 h (B) , 2 h (C) or 4 h (D) . Either 6 h, 12 h, 18 h, or 24 h after infection supernatant was harvested. Virus titer was determined as indicated in the “Materials and Materials” section. Virus titer differed in controls depending on the time the supernatant was harvested after start of treatment. Therefore, only virus titer in percent compared to control is given in this figure, which allows the comparison of all graphs. (E) BAY 81-8781-treatment does not lead to emergence of resistant virus variant upon multiple passaging in cell culture. A549 lung epithelial cells were infected with IAV A/FPV/Bratislava/79 (H7N7) (FPV, fowl plague virus) at a MOI = 0.01 and incubated for 24 h with either BAY 81-8781 (5 mM) or oseltamivir (2 μM). Cell culture supernatants were removed and used to determine viral titers in plaque assays on MDCK cells. Supernatants were adjusted in titers and used for a second infection round in presence or absence of the inhibitors. This procedure was repeated until passage eight. Virus titers are shown relative to titers of untreated control cells (black bars) that were normalized to 100%. p -values of < 0.05 are referred to ∗ .

Journal: Frontiers in Microbiology

Article Title: Pharmacodynamics, Pharmacokinetics, and Antiviral Activity of BAY 81-8781, a Novel NF-κB Inhibiting Anti-influenza Drug

doi: 10.3389/fmicb.2017.02130

Figure Lengend Snippet: Time of addition kinetics with BAY 81-8781 and assessment of emergence of resistance. A549 cells were infected with A/Mallard/Bavaria/1/2006 (MB1) (MOI: 0.001). Twenty-four hours after infection cells were treated with five different concentrations of BAY 81-8781 ranging from 0.001 to 10 mM for either 30 min (A) , 1 h (B) , 2 h (C) or 4 h (D) . Either 6 h, 12 h, 18 h, or 24 h after infection supernatant was harvested. Virus titer was determined as indicated in the “Materials and Materials” section. Virus titer differed in controls depending on the time the supernatant was harvested after start of treatment. Therefore, only virus titer in percent compared to control is given in this figure, which allows the comparison of all graphs. (E) BAY 81-8781-treatment does not lead to emergence of resistant virus variant upon multiple passaging in cell culture. A549 lung epithelial cells were infected with IAV A/FPV/Bratislava/79 (H7N7) (FPV, fowl plague virus) at a MOI = 0.01 and incubated for 24 h with either BAY 81-8781 (5 mM) or oseltamivir (2 μM). Cell culture supernatants were removed and used to determine viral titers in plaque assays on MDCK cells. Supernatants were adjusted in titers and used for a second infection round in presence or absence of the inhibitors. This procedure was repeated until passage eight. Virus titers are shown relative to titers of untreated control cells (black bars) that were normalized to 100%. p -values of < 0.05 are referred to ∗ .

Article Snippet: Thus, BAY 81-8781 treatment showed a greater therapeutic window as Tamiflu ® treatment against infections with a highly pathogenic influenza virus.

Techniques: Infection, Variant Assay, Passaging, Cell Culture, Incubation