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atcc vr  (ATCC)


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    ATCC atcc vr
    Atcc Vr, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 805 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/coronavirus+229e+atcc+vr+740/us12617014-145-39-39?v=ATCC
    Average 96 stars, based on 805 article reviews
    atcc vr - by Bioz Stars, 2026-07
    96/100 stars

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    Identification of host factors involved in SARS-CoV-2 <t>and</t> <t>HCoV-229E</t> replication (A) Schematic overview of the siRNA screening. HEK293 A/T cells were seeded in 24-well plates and transfected twice with siRNAs targeting 91 host genes previously identified as being involved in influenza virus replication. Cells were then infected with SARS-CoV-2 (100 plaque-forming unit [PFU]/100 μL) one day after the second transfection. Supernatants were collected at 2 days post-infection (dpi) and titrated by plaque assay. (B) Results of the SARS-CoV-2 siRNA screen. The 91 host factors were divided into four batches, each including a non-targeting siRNA as a negative control (N) and siRNA targeting SARS-CoV-2 nsp12 as a positive control (P). Viral titers were calculated based on the difference between each siRNA and its corresponding negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± standard deviation (SD) of at least three independent experiments. (C) The seven host factors identified in the SARS-CoV-2 siRNA screen were further examined in HCoV-229E, along with the negative control siRNA (N) and positive control siRNA (P) targeting the HCoV-229E N gene. Following the same method described in (A), MRC-5 cells were infected with HCoV-229E (50 tissue culture infectious dose (TCID 50 )/100 μL). Supernatants were collected at 3 dpi and titrated by TCID 50 assay. Viral titers were calculated based on the difference between each siRNA and the negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± SD of three independent experiments. (D) Cell viability was measured in duplicate wells across two independent experiments using CellTiter-Glo following siRNA transfection. See also and .
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    Identification of host factors involved in SARS-CoV-2 <t>and</t> <t>HCoV-229E</t> replication (A) Schematic overview of the siRNA screening. HEK293 A/T cells were seeded in 24-well plates and transfected twice with siRNAs targeting 91 host genes previously identified as being involved in influenza virus replication. Cells were then infected with SARS-CoV-2 (100 plaque-forming unit [PFU]/100 μL) one day after the second transfection. Supernatants were collected at 2 days post-infection (dpi) and titrated by plaque assay. (B) Results of the SARS-CoV-2 siRNA screen. The 91 host factors were divided into four batches, each including a non-targeting siRNA as a negative control (N) and siRNA targeting SARS-CoV-2 nsp12 as a positive control (P). Viral titers were calculated based on the difference between each siRNA and its corresponding negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± standard deviation (SD) of at least three independent experiments. (C) The seven host factors identified in the SARS-CoV-2 siRNA screen were further examined in HCoV-229E, along with the negative control siRNA (N) and positive control siRNA (P) targeting the HCoV-229E N gene. Following the same method described in (A), MRC-5 cells were infected with HCoV-229E (50 tissue culture infectious dose (TCID 50 )/100 μL). Supernatants were collected at 3 dpi and titrated by TCID 50 assay. Viral titers were calculated based on the difference between each siRNA and the negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± SD of three independent experiments. (D) Cell viability was measured in duplicate wells across two independent experiments using CellTiter-Glo following siRNA transfection. See also and .
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    Identification of host factors involved in SARS-CoV-2 <t>and</t> <t>HCoV-229E</t> replication (A) Schematic overview of the siRNA screening. HEK293 A/T cells were seeded in 24-well plates and transfected twice with siRNAs targeting 91 host genes previously identified as being involved in influenza virus replication. Cells were then infected with SARS-CoV-2 (100 plaque-forming unit [PFU]/100 μL) one day after the second transfection. Supernatants were collected at 2 days post-infection (dpi) and titrated by plaque assay. (B) Results of the SARS-CoV-2 siRNA screen. The 91 host factors were divided into four batches, each including a non-targeting siRNA as a negative control (N) and siRNA targeting SARS-CoV-2 nsp12 as a positive control (P). Viral titers were calculated based on the difference between each siRNA and its corresponding negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± standard deviation (SD) of at least three independent experiments. (C) The seven host factors identified in the SARS-CoV-2 siRNA screen were further examined in HCoV-229E, along with the negative control siRNA (N) and positive control siRNA (P) targeting the HCoV-229E N gene. Following the same method described in (A), MRC-5 cells were infected with HCoV-229E (50 tissue culture infectious dose (TCID 50 )/100 μL). Supernatants were collected at 3 dpi and titrated by TCID 50 assay. Viral titers were calculated based on the difference between each siRNA and the negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± SD of three independent experiments. (D) Cell viability was measured in duplicate wells across two independent experiments using CellTiter-Glo following siRNA transfection. See also and .
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    Identification of host factors involved in SARS-CoV-2 <t>and</t> <t>HCoV-229E</t> replication (A) Schematic overview of the siRNA screening. HEK293 A/T cells were seeded in 24-well plates and transfected twice with siRNAs targeting 91 host genes previously identified as being involved in influenza virus replication. Cells were then infected with SARS-CoV-2 (100 plaque-forming unit [PFU]/100 μL) one day after the second transfection. Supernatants were collected at 2 days post-infection (dpi) and titrated by plaque assay. (B) Results of the SARS-CoV-2 siRNA screen. The 91 host factors were divided into four batches, each including a non-targeting siRNA as a negative control (N) and siRNA targeting SARS-CoV-2 nsp12 as a positive control (P). Viral titers were calculated based on the difference between each siRNA and its corresponding negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± standard deviation (SD) of at least three independent experiments. (C) The seven host factors identified in the SARS-CoV-2 siRNA screen were further examined in HCoV-229E, along with the negative control siRNA (N) and positive control siRNA (P) targeting the HCoV-229E N gene. Following the same method described in (A), MRC-5 cells were infected with HCoV-229E (50 tissue culture infectious dose (TCID 50 )/100 μL). Supernatants were collected at 3 dpi and titrated by TCID 50 assay. Viral titers were calculated based on the difference between each siRNA and the negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± SD of three independent experiments. (D) Cell viability was measured in duplicate wells across two independent experiments using CellTiter-Glo following siRNA transfection. See also and .
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    ATCC e 09 measles virus 1 26 e 06 mumps 1 51 e 06 adenovirus type 1 kb 1 02 e 08 bocavirus k340 1 40 e 09 coronavirus 229e atcc vr
    Identification of host factors involved in SARS-CoV-2 <t>and</t> <t>HCoV-229E</t> replication (A) Schematic overview of the siRNA screening. HEK293 A/T cells were seeded in 24-well plates and transfected twice with siRNAs targeting 91 host genes previously identified as being involved in influenza virus replication. Cells were then infected with SARS-CoV-2 (100 plaque-forming unit [PFU]/100 μL) one day after the second transfection. Supernatants were collected at 2 days post-infection (dpi) and titrated by plaque assay. (B) Results of the SARS-CoV-2 siRNA screen. The 91 host factors were divided into four batches, each including a non-targeting siRNA as a negative control (N) and siRNA targeting SARS-CoV-2 nsp12 as a positive control (P). Viral titers were calculated based on the difference between each siRNA and its corresponding negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± standard deviation (SD) of at least three independent experiments. (C) The seven host factors identified in the SARS-CoV-2 siRNA screen were further examined in HCoV-229E, along with the negative control siRNA (N) and positive control siRNA (P) targeting the HCoV-229E N gene. Following the same method described in (A), MRC-5 cells were infected with HCoV-229E (50 tissue culture infectious dose (TCID 50 )/100 μL). Supernatants were collected at 3 dpi and titrated by TCID 50 assay. Viral titers were calculated based on the difference between each siRNA and the negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± SD of three independent experiments. (D) Cell viability was measured in duplicate wells across two independent experiments using CellTiter-Glo following siRNA transfection. See also and .
    E 09 Measles Virus 1 26 E 06 Mumps 1 51 E 06 Adenovirus Type 1 Kb 1 02 E 08 Bocavirus K340 1 40 E 09 Coronavirus 229e Atcc Vr, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Identification of host factors involved in SARS-CoV-2 <t>and</t> <t>HCoV-229E</t> replication (A) Schematic overview of the siRNA screening. HEK293 A/T cells were seeded in 24-well plates and transfected twice with siRNAs targeting 91 host genes previously identified as being involved in influenza virus replication. Cells were then infected with SARS-CoV-2 (100 plaque-forming unit [PFU]/100 μL) one day after the second transfection. Supernatants were collected at 2 days post-infection (dpi) and titrated by plaque assay. (B) Results of the SARS-CoV-2 siRNA screen. The 91 host factors were divided into four batches, each including a non-targeting siRNA as a negative control (N) and siRNA targeting SARS-CoV-2 nsp12 as a positive control (P). Viral titers were calculated based on the difference between each siRNA and its corresponding negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± standard deviation (SD) of at least three independent experiments. (C) The seven host factors identified in the SARS-CoV-2 siRNA screen were further examined in HCoV-229E, along with the negative control siRNA (N) and positive control siRNA (P) targeting the HCoV-229E N gene. Following the same method described in (A), MRC-5 cells were infected with HCoV-229E (50 tissue culture infectious dose (TCID 50 )/100 μL). Supernatants were collected at 3 dpi and titrated by TCID 50 assay. Viral titers were calculated based on the difference between each siRNA and the negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± SD of three independent experiments. (D) Cell viability was measured in duplicate wells across two independent experiments using CellTiter-Glo following siRNA transfection. See also and .
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    Identification of host factors involved in SARS-CoV-2 <t>and</t> <t>HCoV-229E</t> replication (A) Schematic overview of the siRNA screening. HEK293 A/T cells were seeded in 24-well plates and transfected twice with siRNAs targeting 91 host genes previously identified as being involved in influenza virus replication. Cells were then infected with SARS-CoV-2 (100 plaque-forming unit [PFU]/100 μL) one day after the second transfection. Supernatants were collected at 2 days post-infection (dpi) and titrated by plaque assay. (B) Results of the SARS-CoV-2 siRNA screen. The 91 host factors were divided into four batches, each including a non-targeting siRNA as a negative control (N) and siRNA targeting SARS-CoV-2 nsp12 as a positive control (P). Viral titers were calculated based on the difference between each siRNA and its corresponding negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± standard deviation (SD) of at least three independent experiments. (C) The seven host factors identified in the SARS-CoV-2 siRNA screen were further examined in HCoV-229E, along with the negative control siRNA (N) and positive control siRNA (P) targeting the HCoV-229E N gene. Following the same method described in (A), MRC-5 cells were infected with HCoV-229E (50 tissue culture infectious dose (TCID 50 )/100 μL). Supernatants were collected at 3 dpi and titrated by TCID 50 assay. Viral titers were calculated based on the difference between each siRNA and the negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± SD of three independent experiments. (D) Cell viability was measured in duplicate wells across two independent experiments using CellTiter-Glo following siRNA transfection. See also and .
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    Identification of host factors involved in SARS-CoV-2 <t>and</t> <t>HCoV-229E</t> replication (A) Schematic overview of the siRNA screening. HEK293 A/T cells were seeded in 24-well plates and transfected twice with siRNAs targeting 91 host genes previously identified as being involved in influenza virus replication. Cells were then infected with SARS-CoV-2 (100 plaque-forming unit [PFU]/100 μL) one day after the second transfection. Supernatants were collected at 2 days post-infection (dpi) and titrated by plaque assay. (B) Results of the SARS-CoV-2 siRNA screen. The 91 host factors were divided into four batches, each including a non-targeting siRNA as a negative control (N) and siRNA targeting SARS-CoV-2 nsp12 as a positive control (P). Viral titers were calculated based on the difference between each siRNA and its corresponding negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± standard deviation (SD) of at least three independent experiments. (C) The seven host factors identified in the SARS-CoV-2 siRNA screen were further examined in HCoV-229E, along with the negative control siRNA (N) and positive control siRNA (P) targeting the HCoV-229E N gene. Following the same method described in (A), MRC-5 cells were infected with HCoV-229E (50 tissue culture infectious dose (TCID 50 )/100 μL). Supernatants were collected at 3 dpi and titrated by TCID 50 assay. Viral titers were calculated based on the difference between each siRNA and the negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± SD of three independent experiments. (D) Cell viability was measured in duplicate wells across two independent experiments using CellTiter-Glo following siRNA transfection. See also and .
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    Identification of host factors involved in SARS-CoV-2 and HCoV-229E replication (A) Schematic overview of the siRNA screening. HEK293 A/T cells were seeded in 24-well plates and transfected twice with siRNAs targeting 91 host genes previously identified as being involved in influenza virus replication. Cells were then infected with SARS-CoV-2 (100 plaque-forming unit [PFU]/100 μL) one day after the second transfection. Supernatants were collected at 2 days post-infection (dpi) and titrated by plaque assay. (B) Results of the SARS-CoV-2 siRNA screen. The 91 host factors were divided into four batches, each including a non-targeting siRNA as a negative control (N) and siRNA targeting SARS-CoV-2 nsp12 as a positive control (P). Viral titers were calculated based on the difference between each siRNA and its corresponding negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± standard deviation (SD) of at least three independent experiments. (C) The seven host factors identified in the SARS-CoV-2 siRNA screen were further examined in HCoV-229E, along with the negative control siRNA (N) and positive control siRNA (P) targeting the HCoV-229E N gene. Following the same method described in (A), MRC-5 cells were infected with HCoV-229E (50 tissue culture infectious dose (TCID 50 )/100 μL). Supernatants were collected at 3 dpi and titrated by TCID 50 assay. Viral titers were calculated based on the difference between each siRNA and the negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± SD of three independent experiments. (D) Cell viability was measured in duplicate wells across two independent experiments using CellTiter-Glo following siRNA transfection. See also and .

    Journal: iScience

    Article Title: Broad-spectrum antiviral activity of antisense oligonucleotides targeting GBF1 against SARS-CoV-2 and influenza viruses

    doi: 10.1016/j.isci.2026.114851

    Figure Lengend Snippet: Identification of host factors involved in SARS-CoV-2 and HCoV-229E replication (A) Schematic overview of the siRNA screening. HEK293 A/T cells were seeded in 24-well plates and transfected twice with siRNAs targeting 91 host genes previously identified as being involved in influenza virus replication. Cells were then infected with SARS-CoV-2 (100 plaque-forming unit [PFU]/100 μL) one day after the second transfection. Supernatants were collected at 2 days post-infection (dpi) and titrated by plaque assay. (B) Results of the SARS-CoV-2 siRNA screen. The 91 host factors were divided into four batches, each including a non-targeting siRNA as a negative control (N) and siRNA targeting SARS-CoV-2 nsp12 as a positive control (P). Viral titers were calculated based on the difference between each siRNA and its corresponding negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± standard deviation (SD) of at least three independent experiments. (C) The seven host factors identified in the SARS-CoV-2 siRNA screen were further examined in HCoV-229E, along with the negative control siRNA (N) and positive control siRNA (P) targeting the HCoV-229E N gene. Following the same method described in (A), MRC-5 cells were infected with HCoV-229E (50 tissue culture infectious dose (TCID 50 )/100 μL). Supernatants were collected at 3 dpi and titrated by TCID 50 assay. Viral titers were calculated based on the difference between each siRNA and the negative control. Each dot represents the mean of duplicate wells from a single independent experiment. Data are presented as the mean ± SD of three independent experiments. (D) Cell viability was measured in duplicate wells across two independent experiments using CellTiter-Glo following siRNA transfection. See also and .

    Article Snippet: HCoV-229E , ATCC , VR-740.

    Techniques: Transfection, Virus, Infection, Plaque Assay, Negative Control, Positive Control, Standard Deviation