sendai virus  (ATCC)


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  • 95
    Name:
    Sendai virus Cantell
    Description:

    Catalog Number:
    vr-907
    Price:
    None
    Applications:
    This strain is widely used for induction of interferon and cell fusion.Respiratory research
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    Structured Review

    ATCC sendai virus
    <t>ZIKV</t> NS5 inhibits IRF3 phosphorylation. A. NS5 inhibits polyI:C-induced phosphorylation of IRF3 in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids and, 24 h later, transfected with polyI:C (PIC). Western blotting of phosphor-IRF3 (pIRF3) and total IRF3 was conducted. Relative levels of pIRF3 after PIC stimulation are shown below the images. B. NS5 inhibits <t>Sendai</t> virus-induced IRF3 phosphorylation in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids. At 24 h post transfection, the cells were infected with Sendai virus. The cells were harvested for Western blotting 15 hpi.

    https://www.bioz.com/result/sendai virus/product/ATCC
    Average 95 stars, based on 27 article reviews
    Price from $9.99 to $1999.99
    sendai virus - by Bioz Stars, 2020-09
    95/100 stars

    Images

    1) Product Images from "Zika virus NS5 protein antagonizes type I interferon production via blocking TBK1 activation"

    Article Title: Zika virus NS5 protein antagonizes type I interferon production via blocking TBK1 activation

    Journal: Virology

    doi: 10.1016/j.virol.2018.11.009

    ZIKV NS5 inhibits IRF3 phosphorylation. A. NS5 inhibits polyI:C-induced phosphorylation of IRF3 in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids and, 24 h later, transfected with polyI:C (PIC). Western blotting of phosphor-IRF3 (pIRF3) and total IRF3 was conducted. Relative levels of pIRF3 after PIC stimulation are shown below the images. B. NS5 inhibits Sendai virus-induced IRF3 phosphorylation in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids. At 24 h post transfection, the cells were infected with Sendai virus. The cells were harvested for Western blotting 15 hpi.
    Figure Legend Snippet: ZIKV NS5 inhibits IRF3 phosphorylation. A. NS5 inhibits polyI:C-induced phosphorylation of IRF3 in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids and, 24 h later, transfected with polyI:C (PIC). Western blotting of phosphor-IRF3 (pIRF3) and total IRF3 was conducted. Relative levels of pIRF3 after PIC stimulation are shown below the images. B. NS5 inhibits Sendai virus-induced IRF3 phosphorylation in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids. At 24 h post transfection, the cells were infected with Sendai virus. The cells were harvested for Western blotting 15 hpi.

    Techniques Used: Transfection, Western Blot, Infection

    2) Product Images from "IL-12 p80-dependent macrophage recruitment primes the host for increased survival following a lethal respiratory viral infection"

    Article Title: IL-12 p80-dependent macrophage recruitment primes the host for increased survival following a lethal respiratory viral infection

    Journal: Immunology

    doi: 10.1111/j.1365-2567.2008.02923.x

    Enhanced resolution of viral-dependent airway inflammation in the p80/p40 transgenic mice is associated with altered expression of airway chemokines. (a–d) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated without or with Sendai virus 50 000 egg infectious dose 50% (EID 50 ) and at days 0, 3, 5 and 8 cell-free bronchoalveolar lavage (BAL) supernatants were analysed for CC chemokine ligand 2 (CCL2)/JE [murine homologue of human monocyte chemoattractant protein (MCP)-1] (a), CCL3/macrophage inflammatory protein (MIP)-1α (b), CCL4/MIP-1β (c) and CCL5/RANTES (d). Values represent mean ± standard deviation for duplicate samples ( n = 6–8) and a significant difference from WT is indicated (* P
    Figure Legend Snippet: Enhanced resolution of viral-dependent airway inflammation in the p80/p40 transgenic mice is associated with altered expression of airway chemokines. (a–d) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated without or with Sendai virus 50 000 egg infectious dose 50% (EID 50 ) and at days 0, 3, 5 and 8 cell-free bronchoalveolar lavage (BAL) supernatants were analysed for CC chemokine ligand 2 (CCL2)/JE [murine homologue of human monocyte chemoattractant protein (MCP)-1] (a), CCL3/macrophage inflammatory protein (MIP)-1α (b), CCL4/MIP-1β (c) and CCL5/RANTES (d). Values represent mean ± standard deviation for duplicate samples ( n = 6–8) and a significant difference from WT is indicated (* P

    Techniques Used: Transgenic Assay, Mouse Assay, Expressing, Standard Deviation

    Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is independent of viral load. (a) Wild-type (WT; top) or p80/p40 Tg (bottom) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (50 K) and day 5 post-inoculation lung sections were immunolabelled with anti-Sendai antibody (Ab) [detected with fluorescein isothiocyanate (FITC); green] and anti-CD68 Ab (detected with Alexa Fluor 555; red). Top and bottom rows are identical views photographed with a filter for the green channel (column 1), a filter for the red channel (column 2), and a merged image (column 3). Control immunoglobulin G (IgG) Ab gave no signal above background (not shown). Arrows indicate dual-labelled cells. Representative photomicrographs are shown ( n = 4). Bar, 20 μm. (b) Wild-type (WT) and p80/p40 Tg littermates were inoculated without Sendai virus or with Sendai virus 50 K and day 3, 5, 8 and 12 whole-lung homogenates were analysed for Sendai plaque-forming units (PFU)/g of lung tissue. Values represent mean ± standard deviation for duplicate samples ( n = 6–8). (c) Wild-type and p80/p40 Tg littermates were inoculated without Sendai virus or with Sendai virus 50 K or 5 K and whole-lung RNA from day 3, 5 and 8 post-inoculation was analysed for Sendai virus-specific and GAPDH RNA by one-step fluorogenic reverse transcriptase–polymerase chain reaction (RT-PCR). The mean of duplicate measurements of Sendai virus-specific RNA was normalized to GAPDH and reported as the Sendai to GAPDH ratio. A significant difference from WT is indicated (* P
    Figure Legend Snippet: Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is independent of viral load. (a) Wild-type (WT; top) or p80/p40 Tg (bottom) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (50 K) and day 5 post-inoculation lung sections were immunolabelled with anti-Sendai antibody (Ab) [detected with fluorescein isothiocyanate (FITC); green] and anti-CD68 Ab (detected with Alexa Fluor 555; red). Top and bottom rows are identical views photographed with a filter for the green channel (column 1), a filter for the red channel (column 2), and a merged image (column 3). Control immunoglobulin G (IgG) Ab gave no signal above background (not shown). Arrows indicate dual-labelled cells. Representative photomicrographs are shown ( n = 4). Bar, 20 μm. (b) Wild-type (WT) and p80/p40 Tg littermates were inoculated without Sendai virus or with Sendai virus 50 K and day 3, 5, 8 and 12 whole-lung homogenates were analysed for Sendai plaque-forming units (PFU)/g of lung tissue. Values represent mean ± standard deviation for duplicate samples ( n = 6–8). (c) Wild-type and p80/p40 Tg littermates were inoculated without Sendai virus or with Sendai virus 50 K or 5 K and whole-lung RNA from day 3, 5 and 8 post-inoculation was analysed for Sendai virus-specific and GAPDH RNA by one-step fluorogenic reverse transcriptase–polymerase chain reaction (RT-PCR). The mean of duplicate measurements of Sendai virus-specific RNA was normalized to GAPDH and reported as the Sendai to GAPDH ratio. A significant difference from WT is indicated (* P

    Techniques Used: Infection, Transgenic Assay, Mouse Assay, Standard Deviation, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction

    Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is associated with enhanced resolution of viral-dependent airway inflammation. (a) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (Sendai 50 K) and day 3, 5 and 8 post-inoculation lung sections were stained with haematoxylin and eosin. Representative photomicrographs are shown ( n = 8). Bar, 100 μm. (b–e) BAL from day 3, 5, 8 and 21 post viral inoculation was analysed for total and differential cell numbers. Values represent mean ± standard deviation ( n = 6–8), and a significant difference from WT is indicated (* P
    Figure Legend Snippet: Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is associated with enhanced resolution of viral-dependent airway inflammation. (a) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (Sendai 50 K) and day 3, 5 and 8 post-inoculation lung sections were stained with haematoxylin and eosin. Representative photomicrographs are shown ( n = 8). Bar, 100 μm. (b–e) BAL from day 3, 5, 8 and 21 post viral inoculation was analysed for total and differential cell numbers. Values represent mean ± standard deviation ( n = 6–8), and a significant difference from WT is indicated (* P

    Techniques Used: Infection, Transgenic Assay, Mouse Assay, Staining, Standard Deviation

    Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is abrogated by macrophage depletion. (a) Wild-type (WT; n = 25) or p80/p40 Tg ( n = 21) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (Sendai 50 K) and monitored for survival by Kaplan–Meier analysis. A significant increase in survival of p80/p40 Tg mice (by Wilcoxon rank-sum test) is indicated (* P
    Figure Legend Snippet: Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is abrogated by macrophage depletion. (a) Wild-type (WT; n = 25) or p80/p40 Tg ( n = 21) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (Sendai 50 K) and monitored for survival by Kaplan–Meier analysis. A significant increase in survival of p80/p40 Tg mice (by Wilcoxon rank-sum test) is indicated (* P

    Techniques Used: Infection, Transgenic Assay, Mouse Assay

    Enhanced resolution of viral-dependent airway inflammation in the p80/p40 transgenic mice. (a) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated with Sendai virus 5000 egg infectious dose 50% (Sendai 5 K) and day 3, 5 and 8 post-inoculation lung sections were stained with haematoxylin and eosin. Representative photomicrographs are shown ( n = 5). Bar, 100 μm. (b–e) BAL from day 3, 5, 8 and 21 post viral inoculation was analysed for total and differential cell numbers. Values represent mean ± standard deviation ( n = 4–6), and a significant difference from WT is indicated (* P
    Figure Legend Snippet: Enhanced resolution of viral-dependent airway inflammation in the p80/p40 transgenic mice. (a) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated with Sendai virus 5000 egg infectious dose 50% (Sendai 5 K) and day 3, 5 and 8 post-inoculation lung sections were stained with haematoxylin and eosin. Representative photomicrographs are shown ( n = 5). Bar, 100 μm. (b–e) BAL from day 3, 5, 8 and 21 post viral inoculation was analysed for total and differential cell numbers. Values represent mean ± standard deviation ( n = 4–6), and a significant difference from WT is indicated (* P

    Techniques Used: Transgenic Assay, Mouse Assay, Staining, Standard Deviation

    3) Product Images from "Innate Sensing of HIV-Infected Cells"

    Article Title: Innate Sensing of HIV-Infected Cells

    Journal: PLoS Pathogens

    doi: 10.1371/journal.ppat.1001284

    Sensing of HIV-infected lymphocytes by 293T-derived epithelial cells. a. Role of CD4 and CXCR4 in 293T cells. Activity of the IFNβ promoter in parental 293T cells, and in 293T cells expressing CXCR4 (293T CXCR4), or CD4 and CXCR4 (293T-4X4). These cells were transfected with IFNβ-luciferase reporter plasmid, and cocultivated for 16 h with MT4C5 cells expressing wild-type, ΔEnv, or F552Y HIV. The fold induction of luciferase activity, compared to non-stimulated cells is shown. The paramyxovirus Sendai virus (SeV) was used as a positive control (right panel). b. Role of IRF3. 293T-4X4 cells were transfected with an irrelevant (CTRL) or an anti IRF3 siRNA. 48 h later, cells were cocultivated with HIV-infected MT4C5 cells and assayed for IFN-β promoter activity. Left panel: IRF3 and NFkB levels, assessed by western blot, in control (CTRL) and silenced 293T-4X4 cells. Right panel: IFN-β promoter activity is expressed as a percentage of the signal obtained with control cells (CTRL). SeV, which signals through IRF3, was used as a control. Mean+sd of 3 independent experiments is shown. *p
    Figure Legend Snippet: Sensing of HIV-infected lymphocytes by 293T-derived epithelial cells. a. Role of CD4 and CXCR4 in 293T cells. Activity of the IFNβ promoter in parental 293T cells, and in 293T cells expressing CXCR4 (293T CXCR4), or CD4 and CXCR4 (293T-4X4). These cells were transfected with IFNβ-luciferase reporter plasmid, and cocultivated for 16 h with MT4C5 cells expressing wild-type, ΔEnv, or F552Y HIV. The fold induction of luciferase activity, compared to non-stimulated cells is shown. The paramyxovirus Sendai virus (SeV) was used as a positive control (right panel). b. Role of IRF3. 293T-4X4 cells were transfected with an irrelevant (CTRL) or an anti IRF3 siRNA. 48 h later, cells were cocultivated with HIV-infected MT4C5 cells and assayed for IFN-β promoter activity. Left panel: IRF3 and NFkB levels, assessed by western blot, in control (CTRL) and silenced 293T-4X4 cells. Right panel: IFN-β promoter activity is expressed as a percentage of the signal obtained with control cells (CTRL). SeV, which signals through IRF3, was used as a control. Mean+sd of 3 independent experiments is shown. *p

    Techniques Used: Infection, Derivative Assay, Activity Assay, Expressing, Transfection, Luciferase, Plasmid Preparation, Positive Control, Western Blot

    4) Product Images from "Cell Cycle Arrest in G2/M Phase Enhances Replication of Interferon-Sensitive Cytoplasmic RNA Viruses via Inhibition of Antiviral Gene Expression"

    Article Title: Cell Cycle Arrest in G2/M Phase Enhances Replication of Interferon-Sensitive Cytoplasmic RNA Viruses via Inhibition of Antiviral Gene Expression

    Journal: Journal of Virology

    doi: 10.1128/JVI.01885-18

    G 2 /M arrest improves viral replication only when active type I IFN signaling inhibits viral replication. (A to E) Suit2 cells (A, C, and E), HPAF-II cells (B), or MIA PaCa-2 cells (D) were treated with medium or different concentrations of paclitaxel (Pac) at the indicated concentration ranges for 24 h and then infected (or mock infected) with VSV-ΔM51 (MOI of 0.1 for Suit2 or MOI of 10 for HPAF-II cells), WT VSV (MOI of 0.1), or Sendai virus recombinant SeV-GFP (MOI of 0.1). The MOI for each virus was calculated based on virus titration on BHK-21 cells. The level of GFP intensity was measured in cells over time. (F) BHK-21 cells were treated 26 h prior to or following VSV-ΔM51 infection at an MOI of 0.01 with medium, paclitaxel, colchicine (Col), or ruxolitinib (Ruxo) at the indicated concentration ranges. After infection, virus replication was measured at regular intervals by way of GFP fluorescence. The means and SD of the means are indicated.
    Figure Legend Snippet: G 2 /M arrest improves viral replication only when active type I IFN signaling inhibits viral replication. (A to E) Suit2 cells (A, C, and E), HPAF-II cells (B), or MIA PaCa-2 cells (D) were treated with medium or different concentrations of paclitaxel (Pac) at the indicated concentration ranges for 24 h and then infected (or mock infected) with VSV-ΔM51 (MOI of 0.1 for Suit2 or MOI of 10 for HPAF-II cells), WT VSV (MOI of 0.1), or Sendai virus recombinant SeV-GFP (MOI of 0.1). The MOI for each virus was calculated based on virus titration on BHK-21 cells. The level of GFP intensity was measured in cells over time. (F) BHK-21 cells were treated 26 h prior to or following VSV-ΔM51 infection at an MOI of 0.01 with medium, paclitaxel, colchicine (Col), or ruxolitinib (Ruxo) at the indicated concentration ranges. After infection, virus replication was measured at regular intervals by way of GFP fluorescence. The means and SD of the means are indicated.

    Techniques Used: Concentration Assay, Infection, Recombinant, Titration, Fluorescence

    5) Product Images from "Equine Arteritis Virus Does Not Induce Interferon Production in Equine Endothelial Cells: Identification of Nonstructural Protein 1 as a Main Interferon Antagonist"

    Article Title: Equine Arteritis Virus Does Not Induce Interferon Production in Equine Endothelial Cells: Identification of Nonstructural Protein 1 as a Main Interferon Antagonist

    Journal: BioMed Research International

    doi: 10.1155/2014/420658

    Inhibition of type I IFN production after EAV infection. (a) Expression levels of IFN- β mRNA in EAV infected cells. EECs were mock-infected or infected with EAV VBS at an m.o.i. of 5 for 8 h. Subsequently, cells were infected with Sendai virus (SeV; 100 HAU/mL) for 3 h or 6 h. Total RNA was isolated and real-time RT-PCR was performed for the detection of equine IFN- β . Bar graph showing relative quantitation (RQ) values of IFN- β mRNA expression from three independent experiments are shown. (b) VSV bioassay for IFN production. EECs were mock-infected or infected with EAV VBS at an m.o.i. of 1 for 24 h. SeV was used as an IFN stimulator. Cell culture supernatants were collected and UV-irradiated for 30 min prior to use in the assay. MDBK cells were grown in 96-well plates and incubated with 2-fold dilution series of the supernatant up to 1/32. After 24 h incubation, cells were infected with VSV-GFP at an m.o.i. of 0.1, and 18 h after infection GFP expression was assessed by fluorescence microscopy. Each dilution was tested in duplicate.
    Figure Legend Snippet: Inhibition of type I IFN production after EAV infection. (a) Expression levels of IFN- β mRNA in EAV infected cells. EECs were mock-infected or infected with EAV VBS at an m.o.i. of 5 for 8 h. Subsequently, cells were infected with Sendai virus (SeV; 100 HAU/mL) for 3 h or 6 h. Total RNA was isolated and real-time RT-PCR was performed for the detection of equine IFN- β . Bar graph showing relative quantitation (RQ) values of IFN- β mRNA expression from three independent experiments are shown. (b) VSV bioassay for IFN production. EECs were mock-infected or infected with EAV VBS at an m.o.i. of 1 for 24 h. SeV was used as an IFN stimulator. Cell culture supernatants were collected and UV-irradiated for 30 min prior to use in the assay. MDBK cells were grown in 96-well plates and incubated with 2-fold dilution series of the supernatant up to 1/32. After 24 h incubation, cells were infected with VSV-GFP at an m.o.i. of 0.1, and 18 h after infection GFP expression was assessed by fluorescence microscopy. Each dilution was tested in duplicate.

    Techniques Used: Inhibition, Infection, Expressing, Isolation, Quantitative RT-PCR, Quantitation Assay, Cell Culture, Irradiation, Incubation, Fluorescence, Microscopy

    Related Articles

    Transfection:

    Article Title: Cyclin-dependent kinase activity is required for type I interferon production
    Article Snippet: .. TE671 cells containing stably transfected plasmids with ISRE, or NF-κB promoters driving firefly luciferase were infected with SeV (Cantell Strain; ATCC). .. Luciferase Assay System (Promega) was used to measure luciferase activity on an Omega microplate reader (BMG Labtech).

    Amplification:

    Article Title: An RNA Molecule Derived From Sendai Virus DI Particles Induces Antitumor Immunity and Cancer Cell-selective Apoptosis
    Article Snippet: .. Inactivated Cantell strain HVJ (VR-907 parainfluenza 1 Cantell, Cantell strain from the ATCC) was amplified by the same protocol as the Z strain HVJ described above. .. Instead of UV irradiation, the chorioallantoic fluid that contained Cantell strain HVJ was treated with 0.008% β-propiolactone for 1 hour at room temperature to inactivate the viral replication.

    Luciferase:

    Article Title: Cyclin-dependent kinase activity is required for type I interferon production
    Article Snippet: .. TE671 cells containing stably transfected plasmids with ISRE, or NF-κB promoters driving firefly luciferase were infected with SeV (Cantell Strain; ATCC). .. Luciferase Assay System (Promega) was used to measure luciferase activity on an Omega microplate reader (BMG Labtech).

    Stable Transfection:

    Article Title: Cyclin-dependent kinase activity is required for type I interferon production
    Article Snippet: .. TE671 cells containing stably transfected plasmids with ISRE, or NF-κB promoters driving firefly luciferase were infected with SeV (Cantell Strain; ATCC). .. Luciferase Assay System (Promega) was used to measure luciferase activity on an Omega microplate reader (BMG Labtech).

    Infection:

    Article Title: Cyclin-dependent kinase activity is required for type I interferon production
    Article Snippet: .. TE671 cells containing stably transfected plasmids with ISRE, or NF-κB promoters driving firefly luciferase were infected with SeV (Cantell Strain; ATCC). .. Luciferase Assay System (Promega) was used to measure luciferase activity on an Omega microplate reader (BMG Labtech).

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  • sev  (ATCC)
    95
    ATCC sev
    Neutrophil influx and CXCL2 expression were lower in neonatal lungs . Adult and neonatal C57BL/6 mice were inoculated with <t>SeV</t> 500 <t>pfu/g</t> body weight. a ) On the indicated days, BAL was performed and total BAL fluid cells were counted. b ) To enumerate the neutrophils, BAL fluid cells were subjected to Wright Giemsa staining and differential cell counting. c ) Percentage of neturophils of total BAL cells. d ) Whole lung RNA was analyzed by real-time PCR for CXCL2. * p
    Sev, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 13 article reviews
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    95
    ATCC sendai virus
    <t>ZIKV</t> NS5 inhibits IRF3 phosphorylation. A. NS5 inhibits polyI:C-induced phosphorylation of IRF3 in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids and, 24 h later, transfected with polyI:C (PIC). Western blotting of phosphor-IRF3 (pIRF3) and total IRF3 was conducted. Relative levels of pIRF3 after PIC stimulation are shown below the images. B. NS5 inhibits <t>Sendai</t> virus-induced IRF3 phosphorylation in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids. At 24 h post transfection, the cells were infected with Sendai virus. The cells were harvested for Western blotting 15 hpi.
    Sendai Virus, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sendai virus/product/ATCC
    Average 95 stars, based on 28 article reviews
    Price from $9.99 to $1999.99
    sendai virus - by Bioz Stars, 2020-09
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    Neutrophil influx and CXCL2 expression were lower in neonatal lungs . Adult and neonatal C57BL/6 mice were inoculated with SeV 500 pfu/g body weight. a ) On the indicated days, BAL was performed and total BAL fluid cells were counted. b ) To enumerate the neutrophils, BAL fluid cells were subjected to Wright Giemsa staining and differential cell counting. c ) Percentage of neturophils of total BAL cells. d ) Whole lung RNA was analyzed by real-time PCR for CXCL2. * p

    Journal: Virology Journal

    Article Title: Reduced inflammation and altered innate response in neonates during paramyxoviral infection

    doi: 10.1186/1743-422X-8-549

    Figure Lengend Snippet: Neutrophil influx and CXCL2 expression were lower in neonatal lungs . Adult and neonatal C57BL/6 mice were inoculated with SeV 500 pfu/g body weight. a ) On the indicated days, BAL was performed and total BAL fluid cells were counted. b ) To enumerate the neutrophils, BAL fluid cells were subjected to Wright Giemsa staining and differential cell counting. c ) Percentage of neturophils of total BAL cells. d ) Whole lung RNA was analyzed by real-time PCR for CXCL2. * p

    Article Snippet: Adult mice were anesthetized, and then inoculated intranasally with 500 pfu/g body weight of SeV, strain 52 (American Type Culture Collection) or with UV-inactivated SeV (UV-SeV) in 30 μl sterile PBS.

    Techniques: Expressing, Mouse Assay, Staining, Cell Counting, Real-time Polymerase Chain Reaction

    Neonates had reduced expression of IFN-γ, TNF-γ and CXCL2 even at higher doses of virus . Adult (n = 3 for each dose) and neonatal C57BL/6 mice (n = 6 for each dose) were infected with 50, 500, 5000, or 50,000 pfu SeV/g body weight. a ) Body weight loss in adults b ) Body weights in neonates. White circles 50 pfu/g body weight, black circles 500 pfu/g, white squares 5,000 pfu/g, and black squares 50,000 pfu/g. c ) Adult survival graph: white circles 50 pfu/g (n = 6), black circles 500 pfu/g (n = 6), white squares 5,000 pfu/g (n = 6) black squares 50,000 pfu/g (n = 6). d ) Neonatal survival graph: white circles 50 pfu/g (n = 8), black circles 500 pfu/g (n = 9), white squares 5,000 pfu/g (n = 8) black squares 50,000 pfu/g (n = 7). e ) Post-infection day 7 IFN-γ protein expression was determined by ELISA. * p

    Journal: Virology Journal

    Article Title: Reduced inflammation and altered innate response in neonates during paramyxoviral infection

    doi: 10.1186/1743-422X-8-549

    Figure Lengend Snippet: Neonates had reduced expression of IFN-γ, TNF-γ and CXCL2 even at higher doses of virus . Adult (n = 3 for each dose) and neonatal C57BL/6 mice (n = 6 for each dose) were infected with 50, 500, 5000, or 50,000 pfu SeV/g body weight. a ) Body weight loss in adults b ) Body weights in neonates. White circles 50 pfu/g body weight, black circles 500 pfu/g, white squares 5,000 pfu/g, and black squares 50,000 pfu/g. c ) Adult survival graph: white circles 50 pfu/g (n = 6), black circles 500 pfu/g (n = 6), white squares 5,000 pfu/g (n = 6) black squares 50,000 pfu/g (n = 6). d ) Neonatal survival graph: white circles 50 pfu/g (n = 8), black circles 500 pfu/g (n = 9), white squares 5,000 pfu/g (n = 8) black squares 50,000 pfu/g (n = 7). e ) Post-infection day 7 IFN-γ protein expression was determined by ELISA. * p

    Article Snippet: Adult mice were anesthetized, and then inoculated intranasally with 500 pfu/g body weight of SeV, strain 52 (American Type Culture Collection) or with UV-inactivated SeV (UV-SeV) in 30 μl sterile PBS.

    Techniques: Expressing, Mouse Assay, Infection, Enzyme-linked Immunosorbent Assay

    Adult and neonatal mice displayed differential body weight patterns during viral infection, but had a similar viral load in the lung . a ) 6-8 week old C57BL/6 adult mice (n = 21) were inoculated intranasally with 500 pfu/g body weight SeV in sterile PBS (black squares). The control group was inoculated with an equivalent amount of UV inactivated SeV (white squares). b ) Neonatal C57BL/6 mice (n = 31) were infected on postnatal day 2 with 500 pfu/g body weight SeV (black squares) or with UV-SeV (white squares). c ) Viral plaque assay of whole lung homogenates was performed, and pfu/ml was normalized to weight of the lung tissue (g). d ) Real-time PCR for SeV was performed on whole lung RNA. SeV expression was normalized to GAPDH and percent expression was calculated by the 2(-Delta Delta C(T)) method. Adults (white bars) and neonates (black bars). All values represent means ± SD; SD of adult SeV group was ≤ 1.24. SD of neonatal groups was ≤ 1.10. * s = 0.007, ** p = 0.030

    Journal: Virology Journal

    Article Title: Reduced inflammation and altered innate response in neonates during paramyxoviral infection

    doi: 10.1186/1743-422X-8-549

    Figure Lengend Snippet: Adult and neonatal mice displayed differential body weight patterns during viral infection, but had a similar viral load in the lung . a ) 6-8 week old C57BL/6 adult mice (n = 21) were inoculated intranasally with 500 pfu/g body weight SeV in sterile PBS (black squares). The control group was inoculated with an equivalent amount of UV inactivated SeV (white squares). b ) Neonatal C57BL/6 mice (n = 31) were infected on postnatal day 2 with 500 pfu/g body weight SeV (black squares) or with UV-SeV (white squares). c ) Viral plaque assay of whole lung homogenates was performed, and pfu/ml was normalized to weight of the lung tissue (g). d ) Real-time PCR for SeV was performed on whole lung RNA. SeV expression was normalized to GAPDH and percent expression was calculated by the 2(-Delta Delta C(T)) method. Adults (white bars) and neonates (black bars). All values represent means ± SD; SD of adult SeV group was ≤ 1.24. SD of neonatal groups was ≤ 1.10. * s = 0.007, ** p = 0.030

    Article Snippet: Adult mice were anesthetized, and then inoculated intranasally with 500 pfu/g body weight of SeV, strain 52 (American Type Culture Collection) or with UV-inactivated SeV (UV-SeV) in 30 μl sterile PBS.

    Techniques: Mouse Assay, Infection, Viral Plaque Assay, Real-time Polymerase Chain Reaction, Expressing

    Enhanced resolution of viral-dependent airway inflammation in the p80/p40 transgenic mice is associated with altered expression of airway chemokines. (a–d) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated without or with Sendai virus 50 000 egg infectious dose 50% (EID 50 ) and at days 0, 3, 5 and 8 cell-free bronchoalveolar lavage (BAL) supernatants were analysed for CC chemokine ligand 2 (CCL2)/JE [murine homologue of human monocyte chemoattractant protein (MCP)-1] (a), CCL3/macrophage inflammatory protein (MIP)-1α (b), CCL4/MIP-1β (c) and CCL5/RANTES (d). Values represent mean ± standard deviation for duplicate samples ( n = 6–8) and a significant difference from WT is indicated (* P

    Journal: Immunology

    Article Title: IL-12 p80-dependent macrophage recruitment primes the host for increased survival following a lethal respiratory viral infection

    doi: 10.1111/j.1365-2567.2008.02923.x

    Figure Lengend Snippet: Enhanced resolution of viral-dependent airway inflammation in the p80/p40 transgenic mice is associated with altered expression of airway chemokines. (a–d) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated without or with Sendai virus 50 000 egg infectious dose 50% (EID 50 ) and at days 0, 3, 5 and 8 cell-free bronchoalveolar lavage (BAL) supernatants were analysed for CC chemokine ligand 2 (CCL2)/JE [murine homologue of human monocyte chemoattractant protein (MCP)-1] (a), CCL3/macrophage inflammatory protein (MIP)-1α (b), CCL4/MIP-1β (c) and CCL5/RANTES (d). Values represent mean ± standard deviation for duplicate samples ( n = 6–8) and a significant difference from WT is indicated (* P

    Article Snippet: To assess the role of this increased number of resident airway macrophages in the accumulation of immune cells during a respiratory viral infection, we inoculated the p80/p40 Tg mice with Sendai virus and quantified the BAL immune cells.

    Techniques: Transgenic Assay, Mouse Assay, Expressing, Standard Deviation

    Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is independent of viral load. (a) Wild-type (WT; top) or p80/p40 Tg (bottom) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (50 K) and day 5 post-inoculation lung sections were immunolabelled with anti-Sendai antibody (Ab) [detected with fluorescein isothiocyanate (FITC); green] and anti-CD68 Ab (detected with Alexa Fluor 555; red). Top and bottom rows are identical views photographed with a filter for the green channel (column 1), a filter for the red channel (column 2), and a merged image (column 3). Control immunoglobulin G (IgG) Ab gave no signal above background (not shown). Arrows indicate dual-labelled cells. Representative photomicrographs are shown ( n = 4). Bar, 20 μm. (b) Wild-type (WT) and p80/p40 Tg littermates were inoculated without Sendai virus or with Sendai virus 50 K and day 3, 5, 8 and 12 whole-lung homogenates were analysed for Sendai plaque-forming units (PFU)/g of lung tissue. Values represent mean ± standard deviation for duplicate samples ( n = 6–8). (c) Wild-type and p80/p40 Tg littermates were inoculated without Sendai virus or with Sendai virus 50 K or 5 K and whole-lung RNA from day 3, 5 and 8 post-inoculation was analysed for Sendai virus-specific and GAPDH RNA by one-step fluorogenic reverse transcriptase–polymerase chain reaction (RT-PCR). The mean of duplicate measurements of Sendai virus-specific RNA was normalized to GAPDH and reported as the Sendai to GAPDH ratio. A significant difference from WT is indicated (* P

    Journal: Immunology

    Article Title: IL-12 p80-dependent macrophage recruitment primes the host for increased survival following a lethal respiratory viral infection

    doi: 10.1111/j.1365-2567.2008.02923.x

    Figure Lengend Snippet: Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is independent of viral load. (a) Wild-type (WT; top) or p80/p40 Tg (bottom) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (50 K) and day 5 post-inoculation lung sections were immunolabelled with anti-Sendai antibody (Ab) [detected with fluorescein isothiocyanate (FITC); green] and anti-CD68 Ab (detected with Alexa Fluor 555; red). Top and bottom rows are identical views photographed with a filter for the green channel (column 1), a filter for the red channel (column 2), and a merged image (column 3). Control immunoglobulin G (IgG) Ab gave no signal above background (not shown). Arrows indicate dual-labelled cells. Representative photomicrographs are shown ( n = 4). Bar, 20 μm. (b) Wild-type (WT) and p80/p40 Tg littermates were inoculated without Sendai virus or with Sendai virus 50 K and day 3, 5, 8 and 12 whole-lung homogenates were analysed for Sendai plaque-forming units (PFU)/g of lung tissue. Values represent mean ± standard deviation for duplicate samples ( n = 6–8). (c) Wild-type and p80/p40 Tg littermates were inoculated without Sendai virus or with Sendai virus 50 K or 5 K and whole-lung RNA from day 3, 5 and 8 post-inoculation was analysed for Sendai virus-specific and GAPDH RNA by one-step fluorogenic reverse transcriptase–polymerase chain reaction (RT-PCR). The mean of duplicate measurements of Sendai virus-specific RNA was normalized to GAPDH and reported as the Sendai to GAPDH ratio. A significant difference from WT is indicated (* P

    Article Snippet: To assess the role of this increased number of resident airway macrophages in the accumulation of immune cells during a respiratory viral infection, we inoculated the p80/p40 Tg mice with Sendai virus and quantified the BAL immune cells.

    Techniques: Infection, Transgenic Assay, Mouse Assay, Standard Deviation, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction

    Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is associated with enhanced resolution of viral-dependent airway inflammation. (a) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (Sendai 50 K) and day 3, 5 and 8 post-inoculation lung sections were stained with haematoxylin and eosin. Representative photomicrographs are shown ( n = 8). Bar, 100 μm. (b–e) BAL from day 3, 5, 8 and 21 post viral inoculation was analysed for total and differential cell numbers. Values represent mean ± standard deviation ( n = 6–8), and a significant difference from WT is indicated (* P

    Journal: Immunology

    Article Title: IL-12 p80-dependent macrophage recruitment primes the host for increased survival following a lethal respiratory viral infection

    doi: 10.1111/j.1365-2567.2008.02923.x

    Figure Lengend Snippet: Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is associated with enhanced resolution of viral-dependent airway inflammation. (a) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (Sendai 50 K) and day 3, 5 and 8 post-inoculation lung sections were stained with haematoxylin and eosin. Representative photomicrographs are shown ( n = 8). Bar, 100 μm. (b–e) BAL from day 3, 5, 8 and 21 post viral inoculation was analysed for total and differential cell numbers. Values represent mean ± standard deviation ( n = 6–8), and a significant difference from WT is indicated (* P

    Article Snippet: To assess the role of this increased number of resident airway macrophages in the accumulation of immune cells during a respiratory viral infection, we inoculated the p80/p40 Tg mice with Sendai virus and quantified the BAL immune cells.

    Techniques: Infection, Transgenic Assay, Mouse Assay, Staining, Standard Deviation

    Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is abrogated by macrophage depletion. (a) Wild-type (WT; n = 25) or p80/p40 Tg ( n = 21) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (Sendai 50 K) and monitored for survival by Kaplan–Meier analysis. A significant increase in survival of p80/p40 Tg mice (by Wilcoxon rank-sum test) is indicated (* P

    Journal: Immunology

    Article Title: IL-12 p80-dependent macrophage recruitment primes the host for increased survival following a lethal respiratory viral infection

    doi: 10.1111/j.1365-2567.2008.02923.x

    Figure Lengend Snippet: Resistance to a lethal Sendai virus infection in the p80/p40 transgenic mice is abrogated by macrophage depletion. (a) Wild-type (WT; n = 25) or p80/p40 Tg ( n = 21) littermates were inoculated with Sendai virus 50 000 egg infectious dose 50% (Sendai 50 K) and monitored for survival by Kaplan–Meier analysis. A significant increase in survival of p80/p40 Tg mice (by Wilcoxon rank-sum test) is indicated (* P

    Article Snippet: To assess the role of this increased number of resident airway macrophages in the accumulation of immune cells during a respiratory viral infection, we inoculated the p80/p40 Tg mice with Sendai virus and quantified the BAL immune cells.

    Techniques: Infection, Transgenic Assay, Mouse Assay

    Enhanced resolution of viral-dependent airway inflammation in the p80/p40 transgenic mice. (a) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated with Sendai virus 5000 egg infectious dose 50% (Sendai 5 K) and day 3, 5 and 8 post-inoculation lung sections were stained with haematoxylin and eosin. Representative photomicrographs are shown ( n = 5). Bar, 100 μm. (b–e) BAL from day 3, 5, 8 and 21 post viral inoculation was analysed for total and differential cell numbers. Values represent mean ± standard deviation ( n = 4–6), and a significant difference from WT is indicated (* P

    Journal: Immunology

    Article Title: IL-12 p80-dependent macrophage recruitment primes the host for increased survival following a lethal respiratory viral infection

    doi: 10.1111/j.1365-2567.2008.02923.x

    Figure Lengend Snippet: Enhanced resolution of viral-dependent airway inflammation in the p80/p40 transgenic mice. (a) Wild-type (WT) or p80/p40 transgenic (p80/p40 Tg) littermates were inoculated with Sendai virus 5000 egg infectious dose 50% (Sendai 5 K) and day 3, 5 and 8 post-inoculation lung sections were stained with haematoxylin and eosin. Representative photomicrographs are shown ( n = 5). Bar, 100 μm. (b–e) BAL from day 3, 5, 8 and 21 post viral inoculation was analysed for total and differential cell numbers. Values represent mean ± standard deviation ( n = 4–6), and a significant difference from WT is indicated (* P

    Article Snippet: To assess the role of this increased number of resident airway macrophages in the accumulation of immune cells during a respiratory viral infection, we inoculated the p80/p40 Tg mice with Sendai virus and quantified the BAL immune cells.

    Techniques: Transgenic Assay, Mouse Assay, Staining, Standard Deviation

    ZIKV NS5 inhibits IRF3 phosphorylation. A. NS5 inhibits polyI:C-induced phosphorylation of IRF3 in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids and, 24 h later, transfected with polyI:C (PIC). Western blotting of phosphor-IRF3 (pIRF3) and total IRF3 was conducted. Relative levels of pIRF3 after PIC stimulation are shown below the images. B. NS5 inhibits Sendai virus-induced IRF3 phosphorylation in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids. At 24 h post transfection, the cells were infected with Sendai virus. The cells were harvested for Western blotting 15 hpi.

    Journal: Virology

    Article Title: Zika virus NS5 protein antagonizes type I interferon production via blocking TBK1 activation

    doi: 10.1016/j.virol.2018.11.009

    Figure Lengend Snippet: ZIKV NS5 inhibits IRF3 phosphorylation. A. NS5 inhibits polyI:C-induced phosphorylation of IRF3 in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids and, 24 h later, transfected with polyI:C (PIC). Western blotting of phosphor-IRF3 (pIRF3) and total IRF3 was conducted. Relative levels of pIRF3 after PIC stimulation are shown below the images. B. NS5 inhibits Sendai virus-induced IRF3 phosphorylation in 293-IRF3 cells. The 293-IRF3 cells were transfected with GFP and NS5 plasmids. At 24 h post transfection, the cells were infected with Sendai virus. The cells were harvested for Western blotting 15 hpi.

    Article Snippet: The ZIKV MR766 strain (ATCC VR-84) and Sendai virus (ATCC VR-907) were obtained from the ATCC.

    Techniques: Transfection, Western Blot, Infection

    The HVJ RNA from the DI particle-rich fraction was more efficient than Z or Cantell stain HVJ RNA for promoting cancer cell death and cancer cell-selective induction of Noxa and TRAIL . ( a ) HVJ RNAs were isolated from Z-HVJ-E, β-propiolactone (βPL)-treated

    Journal: Molecular Therapy

    Article Title: An RNA Molecule Derived From Sendai Virus DI Particles Induces Antitumor Immunity and Cancer Cell-selective Apoptosis

    doi: 10.1038/mt.2015.201

    Figure Lengend Snippet: The HVJ RNA from the DI particle-rich fraction was more efficient than Z or Cantell stain HVJ RNA for promoting cancer cell death and cancer cell-selective induction of Noxa and TRAIL . ( a ) HVJ RNAs were isolated from Z-HVJ-E, β-propiolactone (βPL)-treated

    Article Snippet: Inactivated Cantell strain HVJ (VR-907 parainfluenza 1 Cantell, Cantell strain from the ATCC) was amplified by the same protocol as the Z strain HVJ described above.

    Techniques: Staining, Isolation

    Gel-extracted DI RNA was more efficient than Cantell strain HVJ whole-genome RNA for cancer cell killing and the induction of apoptosis-related proteins expression . ( a ) HVJ RNA was isolated from β-propiolactone (βPL)-treated Cantell strain

    Journal: Molecular Therapy

    Article Title: An RNA Molecule Derived From Sendai Virus DI Particles Induces Antitumor Immunity and Cancer Cell-selective Apoptosis

    doi: 10.1038/mt.2015.201

    Figure Lengend Snippet: Gel-extracted DI RNA was more efficient than Cantell strain HVJ whole-genome RNA for cancer cell killing and the induction of apoptosis-related proteins expression . ( a ) HVJ RNA was isolated from β-propiolactone (βPL)-treated Cantell strain

    Article Snippet: Inactivated Cantell strain HVJ (VR-907 parainfluenza 1 Cantell, Cantell strain from the ATCC) was amplified by the same protocol as the Z strain HVJ described above.

    Techniques: Expressing, Isolation

    Inactivated-Cantell strain HVJ stimulated the RIG-I/MAVS signal pathway and proapoptotic proteins expression in cancer cells . ( a ) Inactivated-HVJ RNAs were isolated from UV-irradiated Z strain HVJ (Z-HVJ-E), β-propiolactone (βPL)-treated

    Journal: Molecular Therapy

    Article Title: An RNA Molecule Derived From Sendai Virus DI Particles Induces Antitumor Immunity and Cancer Cell-selective Apoptosis

    doi: 10.1038/mt.2015.201

    Figure Lengend Snippet: Inactivated-Cantell strain HVJ stimulated the RIG-I/MAVS signal pathway and proapoptotic proteins expression in cancer cells . ( a ) Inactivated-HVJ RNAs were isolated from UV-irradiated Z strain HVJ (Z-HVJ-E), β-propiolactone (βPL)-treated

    Article Snippet: Inactivated Cantell strain HVJ (VR-907 parainfluenza 1 Cantell, Cantell strain from the ATCC) was amplified by the same protocol as the Z strain HVJ described above.

    Techniques: Expressing, Isolation, Irradiation