Structured Review

Innogenetics hcv rna
Effect of <t>HCV,</t> HCV-LPs, HCV core, and envelope glycoprotein E2 on the secretion of IFN-α from pDCs stimulated with TLR7 or TLR9 agonists. (A) Purified pDCs were exposed to 100, 10, or 1 HCVcc <t>RNA</t> copies per cell or to patient sera-derived HCV. Alternatively, pDCs were primed with the same quantity of virus inactivated with heat-treatment at 56°C for 30 min (HCVcc, 56°C) or with UV-treatment at 0.2 J/cm 2 (HCVcc, UV), or exposed to noninfectious insect cell-derived HCV-LPs (0.1 µg E2/ml corresponding to approximately 5,000 particles per cell) or to control (ctrl) cell preparations (1 µg/ml). pDC were also incubated with HCV core or envelope glycoprotein E2 (10 µg/ml), or with an equivalent volume of control supernatant collected 16 h after UV irradiation of Huh7.5 cells transfected with HCV subgenomic replicon at 30 mJ/cm 2 prepared in the same way as the viral stock (Sg-replicon, UV). pDCs were also primed with HCV virus particles (100 HCV genomes per cell) prepared from five different sera of chronically infected patients (HCV + serum) or from equivalent volumes of four different sera of healthy individuals (HCV − serum). Two hours later, primed or mock-primed pDCs were stimulated (A) with TLR9-agonists, with CpG-A (2.5 µg/ml), or with HHV-1 KOS (multiplicity of infection = 100), or (C) with TLR7-agonists, with resiquimod (R848, 0.5-µM), or with influenza virus A/H3N2/Johannesburg (multiplicity of infection = 100). Secretion of IFN-α (A, C) or TNF-α (B) in cell-free supernatant of pDCs was determined by means of ELISA analysis 1 day post-stimulation. The results are expressed as percentages of IFN-α production from pDCs that were first primed as specified above and then further treated with the respective TLR agonist relative to IFN-α production from pDCs stimulated only with the respective TLR agonist. p W , Wilcoxon matched pairs test used to compare differences between the distributions of IFN-α production in primed and non-primed pDC-cultures; p M-W , Mann-Whitney two-tailed non-parametric test used to compare differences between the distributions of IFN-α production in HCV-exposed and Sg-replicon-exposed pDC cultures, or in HCV + serum-exposed and HCV − serum-exposed pDC cultures.
Hcv Rna, supplied by Innogenetics, used in various techniques. Bioz Stars score: 92/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hcv rna/product/Innogenetics
Average 92 stars, based on 5 article reviews
Price from $9.99 to $1999.99
hcv rna - by Bioz Stars, 2020-05
92/100 stars

Images

1) Product Images from "Hepatitis C Virus Is a Weak Inducer of Interferon Alpha in Plasmacytoid Dendritic Cells in Comparison with Influenza and Human Herpesvirus Type-1"

Article Title: Hepatitis C Virus Is a Weak Inducer of Interferon Alpha in Plasmacytoid Dendritic Cells in Comparison with Influenza and Human Herpesvirus Type-1

Journal: PLoS ONE

doi: 10.1371/journal.pone.0004319

Effect of HCV, HCV-LPs, HCV core, and envelope glycoprotein E2 on the secretion of IFN-α from pDCs stimulated with TLR7 or TLR9 agonists. (A) Purified pDCs were exposed to 100, 10, or 1 HCVcc RNA copies per cell or to patient sera-derived HCV. Alternatively, pDCs were primed with the same quantity of virus inactivated with heat-treatment at 56°C for 30 min (HCVcc, 56°C) or with UV-treatment at 0.2 J/cm 2 (HCVcc, UV), or exposed to noninfectious insect cell-derived HCV-LPs (0.1 µg E2/ml corresponding to approximately 5,000 particles per cell) or to control (ctrl) cell preparations (1 µg/ml). pDC were also incubated with HCV core or envelope glycoprotein E2 (10 µg/ml), or with an equivalent volume of control supernatant collected 16 h after UV irradiation of Huh7.5 cells transfected with HCV subgenomic replicon at 30 mJ/cm 2 prepared in the same way as the viral stock (Sg-replicon, UV). pDCs were also primed with HCV virus particles (100 HCV genomes per cell) prepared from five different sera of chronically infected patients (HCV + serum) or from equivalent volumes of four different sera of healthy individuals (HCV − serum). Two hours later, primed or mock-primed pDCs were stimulated (A) with TLR9-agonists, with CpG-A (2.5 µg/ml), or with HHV-1 KOS (multiplicity of infection = 100), or (C) with TLR7-agonists, with resiquimod (R848, 0.5-µM), or with influenza virus A/H3N2/Johannesburg (multiplicity of infection = 100). Secretion of IFN-α (A, C) or TNF-α (B) in cell-free supernatant of pDCs was determined by means of ELISA analysis 1 day post-stimulation. The results are expressed as percentages of IFN-α production from pDCs that were first primed as specified above and then further treated with the respective TLR agonist relative to IFN-α production from pDCs stimulated only with the respective TLR agonist. p W , Wilcoxon matched pairs test used to compare differences between the distributions of IFN-α production in primed and non-primed pDC-cultures; p M-W , Mann-Whitney two-tailed non-parametric test used to compare differences between the distributions of IFN-α production in HCV-exposed and Sg-replicon-exposed pDC cultures, or in HCV + serum-exposed and HCV − serum-exposed pDC cultures.
Figure Legend Snippet: Effect of HCV, HCV-LPs, HCV core, and envelope glycoprotein E2 on the secretion of IFN-α from pDCs stimulated with TLR7 or TLR9 agonists. (A) Purified pDCs were exposed to 100, 10, or 1 HCVcc RNA copies per cell or to patient sera-derived HCV. Alternatively, pDCs were primed with the same quantity of virus inactivated with heat-treatment at 56°C for 30 min (HCVcc, 56°C) or with UV-treatment at 0.2 J/cm 2 (HCVcc, UV), or exposed to noninfectious insect cell-derived HCV-LPs (0.1 µg E2/ml corresponding to approximately 5,000 particles per cell) or to control (ctrl) cell preparations (1 µg/ml). pDC were also incubated with HCV core or envelope glycoprotein E2 (10 µg/ml), or with an equivalent volume of control supernatant collected 16 h after UV irradiation of Huh7.5 cells transfected with HCV subgenomic replicon at 30 mJ/cm 2 prepared in the same way as the viral stock (Sg-replicon, UV). pDCs were also primed with HCV virus particles (100 HCV genomes per cell) prepared from five different sera of chronically infected patients (HCV + serum) or from equivalent volumes of four different sera of healthy individuals (HCV − serum). Two hours later, primed or mock-primed pDCs were stimulated (A) with TLR9-agonists, with CpG-A (2.5 µg/ml), or with HHV-1 KOS (multiplicity of infection = 100), or (C) with TLR7-agonists, with resiquimod (R848, 0.5-µM), or with influenza virus A/H3N2/Johannesburg (multiplicity of infection = 100). Secretion of IFN-α (A, C) or TNF-α (B) in cell-free supernatant of pDCs was determined by means of ELISA analysis 1 day post-stimulation. The results are expressed as percentages of IFN-α production from pDCs that were first primed as specified above and then further treated with the respective TLR agonist relative to IFN-α production from pDCs stimulated only with the respective TLR agonist. p W , Wilcoxon matched pairs test used to compare differences between the distributions of IFN-α production in primed and non-primed pDC-cultures; p M-W , Mann-Whitney two-tailed non-parametric test used to compare differences between the distributions of IFN-α production in HCV-exposed and Sg-replicon-exposed pDC cultures, or in HCV + serum-exposed and HCV − serum-exposed pDC cultures.

Techniques Used: Purification, Derivative Assay, Incubation, Irradiation, Transfection, Infection, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY, Two Tailed Test

Kinetics of disruption of CpG-A-mediated stimulation of pDCs with HCVcc. (A) Flow chart protocol showing inoculation with HCV (solid arrows), treatment with CpG-A (dashed arrows), and IFN-α assay determined by ELISA. (B) Percentage of IFN-α secreted by pDCs that were stimulated with CpG-A and HCV relative to IFN-α secretion by pDCs stimulated only with CpG-A. Purified pDCs were inoculated with 100 HCVcc RNA copies per cell. (C) Effect of HCVcc on the expression of IFN-α, IRF-7, TLR7 and TLR9 mRNA. pDCs were primed with HCVcc and stimulated with CpG-A as shown in panel A, line a . The gene expression levels were determined with real-time PCR were normalized to GAPDH expression. Data are presented as fold induction over medium control at time zero (given the value of 1.0) and are from one of three representative experiments.
Figure Legend Snippet: Kinetics of disruption of CpG-A-mediated stimulation of pDCs with HCVcc. (A) Flow chart protocol showing inoculation with HCV (solid arrows), treatment with CpG-A (dashed arrows), and IFN-α assay determined by ELISA. (B) Percentage of IFN-α secreted by pDCs that were stimulated with CpG-A and HCV relative to IFN-α secretion by pDCs stimulated only with CpG-A. Purified pDCs were inoculated with 100 HCVcc RNA copies per cell. (C) Effect of HCVcc on the expression of IFN-α, IRF-7, TLR7 and TLR9 mRNA. pDCs were primed with HCVcc and stimulated with CpG-A as shown in panel A, line a . The gene expression levels were determined with real-time PCR were normalized to GAPDH expression. Data are presented as fold induction over medium control at time zero (given the value of 1.0) and are from one of three representative experiments.

Techniques Used: Flow Cytometry, Enzyme-linked Immunosorbent Assay, Purification, Expressing, Real-time Polymerase Chain Reaction

Secretion of IFN-α induced with cell culture-derived HCVcc and patient-derived HCV in pDCs from different normal healthy donors. Purified pDCs were inoculated with different quantities of HCVcc (genotype 2) or patient-derived HCV (genotypes 1a, 1b, 2a, and 3a). Viral genomes were quantified by semiquantitative RT-PCR. As negative control, a suspension prepared from cell-free supernatant of Huh7.5 cells transfected with HCV subgenomic (sg) replicon was used. This negative control suspension was concentrated and purified in the same manner as the viral suspension used for exposure of pDCs to 100 genome-containing virus particles per cell. Resiquimod (R848, 0.5 µM) was used as a positive control. Cell cultures of pDCs purified from different normal healthy donors adjusted to a concentration of 10 6 cells/ml in the presence of IL-3 were inoculated with HCV (quantified by HCV RNA copies) in a total volume of 200 µl. Secretion of IFN-α in cell-free supernatant was determined by ELISA 1 day post-stimulation. Identical symbols at a given multiplicity of infection indicate results with pDCs of different donors.
Figure Legend Snippet: Secretion of IFN-α induced with cell culture-derived HCVcc and patient-derived HCV in pDCs from different normal healthy donors. Purified pDCs were inoculated with different quantities of HCVcc (genotype 2) or patient-derived HCV (genotypes 1a, 1b, 2a, and 3a). Viral genomes were quantified by semiquantitative RT-PCR. As negative control, a suspension prepared from cell-free supernatant of Huh7.5 cells transfected with HCV subgenomic (sg) replicon was used. This negative control suspension was concentrated and purified in the same manner as the viral suspension used for exposure of pDCs to 100 genome-containing virus particles per cell. Resiquimod (R848, 0.5 µM) was used as a positive control. Cell cultures of pDCs purified from different normal healthy donors adjusted to a concentration of 10 6 cells/ml in the presence of IL-3 were inoculated with HCV (quantified by HCV RNA copies) in a total volume of 200 µl. Secretion of IFN-α in cell-free supernatant was determined by ELISA 1 day post-stimulation. Identical symbols at a given multiplicity of infection indicate results with pDCs of different donors.

Techniques Used: Cell Culture, Derivative Assay, Purification, Reverse Transcription Polymerase Chain Reaction, Negative Control, Transfection, Positive Control, Concentration Assay, Enzyme-linked Immunosorbent Assay, Infection

2) Product Images from "Human Monoclonal Antibodies That Inhibit Binding of Hepatitis C Virus E2 Protein to CD81 and Recognize Conserved Conformational Epitopes"

Article Title: Human Monoclonal Antibodies That Inhibit Binding of Hepatitis C Virus E2 Protein to CD81 and Recognize Conserved Conformational Epitopes

Journal: Journal of Virology

doi:

HMAbs CBH-2 and CBH-5 inhibit binding of HCV virions to CD81. Number of HCV RNA molecules bound to polystyrene beads ( x axis) after HCV 1a chimpanzee serum was combined with 10 μg of the indicated antibodies ( y axis) and then allowed to bind to beads coated with CD81-LEL. The virion binding experiment was performed as described in Materials and Methods.
Figure Legend Snippet: HMAbs CBH-2 and CBH-5 inhibit binding of HCV virions to CD81. Number of HCV RNA molecules bound to polystyrene beads ( x axis) after HCV 1a chimpanzee serum was combined with 10 μg of the indicated antibodies ( y axis) and then allowed to bind to beads coated with CD81-LEL. The virion binding experiment was performed as described in Materials and Methods.

Techniques Used: Binding Assay

3) Product Images from "Occult Hepatitis C Virus Infection in Candidates for Liver Transplant With Cryptogenic Cirrhosis"

Article Title: Occult Hepatitis C Virus Infection in Candidates for Liver Transplant With Cryptogenic Cirrhosis

Journal: Hepatitis Monthly

doi: 10.5812/hepatmon.11290

Result of HCV RNA Detection by RT Nested-PCR Method Lane1: 100 bp DNA ladder, Lane 2: PCR products of first patient's serum, Lane 3: PCR products of first patient's PBMCs, Lane 4: PCR products of second patient's serum, Lane 5: PCR products of second patient's PBMCs, Lane 6: Negative control in RT round PCR, Lane 7: Negative control in first round PCR, Lane 8: Negative control in second round PCR, Lane 9: HCV RNA positive control, Lane 10: HCV RNA negative control, Lane 11: 100 bp DNA ladder.
Figure Legend Snippet: Result of HCV RNA Detection by RT Nested-PCR Method Lane1: 100 bp DNA ladder, Lane 2: PCR products of first patient's serum, Lane 3: PCR products of first patient's PBMCs, Lane 4: PCR products of second patient's serum, Lane 5: PCR products of second patient's PBMCs, Lane 6: Negative control in RT round PCR, Lane 7: Negative control in first round PCR, Lane 8: Negative control in second round PCR, Lane 9: HCV RNA positive control, Lane 10: HCV RNA negative control, Lane 11: 100 bp DNA ladder.

Techniques Used: RNA Detection, Nested PCR, Polymerase Chain Reaction, Negative Control, Positive Control

4) Product Images from "Hepatitis C virus core, NS3, NS4B and NS5A are the major immunogenic proteins in humoral immunity in chronic HCV infection"

Article Title: Hepatitis C virus core, NS3, NS4B and NS5A are the major immunogenic proteins in humoral immunity in chronic HCV infection

Journal: Virology Journal

doi: 10.1186/1743-422X-6-84

Detection of anti-HCV antibodies in HCV RNA and antibody positive human sera with recombinant HCV proteins . 1 μg of each baculovirus-expressed and preparative SDS-PAGE-purified recombinant HCV protein was loaded onto 10–20% Tris-glycine polyacrylamide gradient gels. Core, NS2, NS3, NS4A, NS4B, and NS5A were loaded on one gel, and E1, E2, and NS5B on another gel, respectively. 3 μg of Sf 9 cell extract was also loaded onto one gel as a control. Proteins separated on gels were transferred to nylon membranes, sliced and stained with serially diluted human serum obtained from HCV RNA and antibody positive patients. The following dilutions were used (lane 1) 1:100, (lane 2) 1:500, (lane 3) 1:2500, (lane 4) 1:12500 and 1:62500 (not shown). After incubation with secondary Abs, the bands were visualized by 3-amino-9-ethylcarbazole (AEC). A. An example of highly positive human serum number 36 is shown, B. an example of a weakly positive human serum number 17 is shown.
Figure Legend Snippet: Detection of anti-HCV antibodies in HCV RNA and antibody positive human sera with recombinant HCV proteins . 1 μg of each baculovirus-expressed and preparative SDS-PAGE-purified recombinant HCV protein was loaded onto 10–20% Tris-glycine polyacrylamide gradient gels. Core, NS2, NS3, NS4A, NS4B, and NS5A were loaded on one gel, and E1, E2, and NS5B on another gel, respectively. 3 μg of Sf 9 cell extract was also loaded onto one gel as a control. Proteins separated on gels were transferred to nylon membranes, sliced and stained with serially diluted human serum obtained from HCV RNA and antibody positive patients. The following dilutions were used (lane 1) 1:100, (lane 2) 1:500, (lane 3) 1:2500, (lane 4) 1:12500 and 1:62500 (not shown). After incubation with secondary Abs, the bands were visualized by 3-amino-9-ethylcarbazole (AEC). A. An example of highly positive human serum number 36 is shown, B. an example of a weakly positive human serum number 17 is shown.

Techniques Used: Recombinant, SDS Page, Purification, Staining, Incubation

The persistence of anti-HCV antibody responses against individual HCV proteins . HCV antibody prevalence in five HCV RNA and antibody positive individuals infected with genotype 1b or 3a was analyzed from serum specimens obtained before and after IFN-α monotherapy (black bar). Relative anti-HCV antibody titers were determined by Western blot analysis as described in Fig. 2.
Figure Legend Snippet: The persistence of anti-HCV antibody responses against individual HCV proteins . HCV antibody prevalence in five HCV RNA and antibody positive individuals infected with genotype 1b or 3a was analyzed from serum specimens obtained before and after IFN-α monotherapy (black bar). Relative anti-HCV antibody titers were determined by Western blot analysis as described in Fig. 2.

Techniques Used: Infection, Western Blot

The specificity of anti-HCV antibody responses in patients suffering from chronic HCV infection . A. The frequency of antibodies against individual recombinant HCV proteins in 68 serum specimens obtained from patients suffering from chronic HCV infection. Both the number and percentage of positive sera are shown. B. The relative antibody levels against individual HCV proteins were determined as the last serum dilution showing a positive signal in Western blot analysis. The means and standard deviations of the means for antibody levels against individual HCV proteins are shown based on 68 HCV RNA and antibody positive patient sera. Only individuals showing a positive antibody response against a given HCV protein are included into the means.
Figure Legend Snippet: The specificity of anti-HCV antibody responses in patients suffering from chronic HCV infection . A. The frequency of antibodies against individual recombinant HCV proteins in 68 serum specimens obtained from patients suffering from chronic HCV infection. Both the number and percentage of positive sera are shown. B. The relative antibody levels against individual HCV proteins were determined as the last serum dilution showing a positive signal in Western blot analysis. The means and standard deviations of the means for antibody levels against individual HCV proteins are shown based on 68 HCV RNA and antibody positive patient sera. Only individuals showing a positive antibody response against a given HCV protein are included into the means.

Techniques Used: Infection, Recombinant, Western Blot

Related Articles

Amplification:

Article Title: Occult Hepatitis C Virus Infection in Candidates for Liver Transplant With Cryptogenic Cirrhosis
Article Snippet: .. The 5′-UTR genotyping of HCV RNA amplified from PBMC specimens was performed by the INNO-LiPATM HCV II kit (Innogenetics, Ghent, Belgium) according to the manufacturer’s instructions. .. This HCV genotyping was also confirmed by sequencing 5′-UTR fragments after the PCR products were cloned into the pJET1.2/blunt cloning vector (Fermentas, St. Leon-Rot, Germany) as described elsewhere ( , ) ( ).

Article Title: Serum Immunoglobulin G Antibodies to the GOR Autoepitope Are Present in Patients with Occult Hepatitis C Virus (HCV) Infection despite Lack of HCV-Specific Antibodies ▿
Article Snippet: .. The HCV RNA amplified from liver biopsy specimens was genotyped by a standard method (Inno-LIPA HCV II; Innogenetics); all patients with occult HCV infection were infected with HCV genotype 1b ( ). .. Other known causes of liver disease were excluded on the basis of clinical, epidemiological, and laboratory data: infection with hepatitis B virus (HBV; hepatitis B surface antigen and serum HBV DNA negative), autoimmunity (negativity for antinuclear and antimitochondrial antibodies, etc.), metabolic and genetic disorders, alcohol intake, drug toxicity, etc.

Article Title: Hepatitis B virus infection in Haemodialysis Centres from Santa Catarina State, Southern Brazil. Predictive risk factors for infection and molecular epidemiology
Article Snippet: .. HCV RNA was detected by a commercial RT-PCR kit following the manufacturer recommendations (INNO-LiPA HCVII PCR amplification, Innogenetics, Ghent, Belgium). .. Sequencing reactions PCR products covering the S gene were submitted to cycle sequencing reactions, using the second round primers and a method derived from Sanger et al. [ ] with dideoxinucleotides (ddNTPs) labelled with fluorescent markers (ABI PrismR BigDyeTM Terminator Cycle Sequencing Ready Reaction Kit – Applied Biosystems, Foster City, CA, USA).

Infection:

Article Title: Serum Immunoglobulin G Antibodies to the GOR Autoepitope Are Present in Patients with Occult Hepatitis C Virus (HCV) Infection despite Lack of HCV-Specific Antibodies ▿
Article Snippet: .. The HCV RNA amplified from liver biopsy specimens was genotyped by a standard method (Inno-LIPA HCV II; Innogenetics); all patients with occult HCV infection were infected with HCV genotype 1b ( ). .. Other known causes of liver disease were excluded on the basis of clinical, epidemiological, and laboratory data: infection with hepatitis B virus (HBV; hepatitis B surface antigen and serum HBV DNA negative), autoimmunity (negativity for antinuclear and antimitochondrial antibodies, etc.), metabolic and genetic disorders, alcohol intake, drug toxicity, etc.

Real-time Polymerase Chain Reaction:

Article Title: Rheumatoid arthritis following PEG-interferon-alfa-2a plus ribavirin treatment for chronic hepatitis C: a case report and review of the literature
Article Snippet: .. HCV RNA was 660,000 IU/mL (TaqMan Real Time PCR); HCV genotype was 3a (INNO-LiPA HCV; Innogenetics, Ghent, Belgium). ..

Reverse Transcription Polymerase Chain Reaction:

Article Title: Natural evolution of hepatitis C virus infection in hemodialysis Tunisian patients and CTLA-4 SNP's
Article Snippet: .. HCV RNA in serum was detected by RT-PCR (Inno-Lipa HCV II, Innogenetics, Belgium) according to the manufacturer’s instructions. ..

Article Title: Hepatitis B virus infection in Haemodialysis Centres from Santa Catarina State, Southern Brazil. Predictive risk factors for infection and molecular epidemiology
Article Snippet: .. HCV RNA was detected by a commercial RT-PCR kit following the manufacturer recommendations (INNO-LiPA HCVII PCR amplification, Innogenetics, Ghent, Belgium). .. Sequencing reactions PCR products covering the S gene were submitted to cycle sequencing reactions, using the second round primers and a method derived from Sanger et al. [ ] with dideoxinucleotides (ddNTPs) labelled with fluorescent markers (ABI PrismR BigDyeTM Terminator Cycle Sequencing Ready Reaction Kit – Applied Biosystems, Foster City, CA, USA).

other:

Article Title: Hepatitis C Virus Is a Weak Inducer of Interferon Alpha in Plasmacytoid Dendritic Cells in Comparison with Influenza and Human Herpesvirus Type-1
Article Snippet: We quantified and genotyped HCV RNA from each serum sample using a branched DNA assay (Quantiplex HCV RNA 2.0 assay; Chiron Diagnostics) and a line probe assay (Inno-LiPA HCVII; Innogenetics), respectively.

Polymerase Chain Reaction:

Article Title: Hepatitis B virus infection in Haemodialysis Centres from Santa Catarina State, Southern Brazil. Predictive risk factors for infection and molecular epidemiology
Article Snippet: .. HCV RNA was detected by a commercial RT-PCR kit following the manufacturer recommendations (INNO-LiPA HCVII PCR amplification, Innogenetics, Ghent, Belgium). .. Sequencing reactions PCR products covering the S gene were submitted to cycle sequencing reactions, using the second round primers and a method derived from Sanger et al. [ ] with dideoxinucleotides (ddNTPs) labelled with fluorescent markers (ABI PrismR BigDyeTM Terminator Cycle Sequencing Ready Reaction Kit – Applied Biosystems, Foster City, CA, USA).

Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 88
    Innogenetics hcv rna quantitation
    <t>HCV-RNA</t> levels during treatment and follow-up.
    Hcv Rna Quantitation, supplied by Innogenetics, used in various techniques. Bioz Stars score: 88/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hcv rna quantitation/product/Innogenetics
    Average 88 stars, based on 7 article reviews
    Price from $9.99 to $1999.99
    hcv rna quantitation - by Bioz Stars, 2020-05
    88/100 stars
      Buy from Supplier

    Image Search Results


    HCV-RNA levels during treatment and follow-up.

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: Use of Fluoroquinolones in Patients with Chronic Hepatitis C Virus-Induced Liver Failure

    doi: 10.1128/AAC.46.10.3280-3282.2002

    Figure Lengend Snippet: HCV-RNA levels during treatment and follow-up.

    Article Snippet: At each visit, sera were tested for liver enzymes (alanine and aspartate aminotransferases, alkaline phosphatase, and glutamyltransferase) and function tests (albumin, bilirubin, and prothrombin time/international normalized ratio) by standard laboratory procedures while stored sera were batched and tested for HCV-RNA quantitation by real-time PCR (see below) and genotyping by line probe assay (INNO-LiPA HCV II; Innogenetics, Toronto, Canada).

    Techniques:

    Effect of HCV, HCV-LPs, HCV core, and envelope glycoprotein E2 on the secretion of IFN-α from pDCs stimulated with TLR7 or TLR9 agonists. (A) Purified pDCs were exposed to 100, 10, or 1 HCVcc RNA copies per cell or to patient sera-derived HCV. Alternatively, pDCs were primed with the same quantity of virus inactivated with heat-treatment at 56°C for 30 min (HCVcc, 56°C) or with UV-treatment at 0.2 J/cm 2 (HCVcc, UV), or exposed to noninfectious insect cell-derived HCV-LPs (0.1 µg E2/ml corresponding to approximately 5,000 particles per cell) or to control (ctrl) cell preparations (1 µg/ml). pDC were also incubated with HCV core or envelope glycoprotein E2 (10 µg/ml), or with an equivalent volume of control supernatant collected 16 h after UV irradiation of Huh7.5 cells transfected with HCV subgenomic replicon at 30 mJ/cm 2 prepared in the same way as the viral stock (Sg-replicon, UV). pDCs were also primed with HCV virus particles (100 HCV genomes per cell) prepared from five different sera of chronically infected patients (HCV + serum) or from equivalent volumes of four different sera of healthy individuals (HCV − serum). Two hours later, primed or mock-primed pDCs were stimulated (A) with TLR9-agonists, with CpG-A (2.5 µg/ml), or with HHV-1 KOS (multiplicity of infection = 100), or (C) with TLR7-agonists, with resiquimod (R848, 0.5-µM), or with influenza virus A/H3N2/Johannesburg (multiplicity of infection = 100). Secretion of IFN-α (A, C) or TNF-α (B) in cell-free supernatant of pDCs was determined by means of ELISA analysis 1 day post-stimulation. The results are expressed as percentages of IFN-α production from pDCs that were first primed as specified above and then further treated with the respective TLR agonist relative to IFN-α production from pDCs stimulated only with the respective TLR agonist. p W , Wilcoxon matched pairs test used to compare differences between the distributions of IFN-α production in primed and non-primed pDC-cultures; p M-W , Mann-Whitney two-tailed non-parametric test used to compare differences between the distributions of IFN-α production in HCV-exposed and Sg-replicon-exposed pDC cultures, or in HCV + serum-exposed and HCV − serum-exposed pDC cultures.

    Journal: PLoS ONE

    Article Title: Hepatitis C Virus Is a Weak Inducer of Interferon Alpha in Plasmacytoid Dendritic Cells in Comparison with Influenza and Human Herpesvirus Type-1

    doi: 10.1371/journal.pone.0004319

    Figure Lengend Snippet: Effect of HCV, HCV-LPs, HCV core, and envelope glycoprotein E2 on the secretion of IFN-α from pDCs stimulated with TLR7 or TLR9 agonists. (A) Purified pDCs were exposed to 100, 10, or 1 HCVcc RNA copies per cell or to patient sera-derived HCV. Alternatively, pDCs were primed with the same quantity of virus inactivated with heat-treatment at 56°C for 30 min (HCVcc, 56°C) or with UV-treatment at 0.2 J/cm 2 (HCVcc, UV), or exposed to noninfectious insect cell-derived HCV-LPs (0.1 µg E2/ml corresponding to approximately 5,000 particles per cell) or to control (ctrl) cell preparations (1 µg/ml). pDC were also incubated with HCV core or envelope glycoprotein E2 (10 µg/ml), or with an equivalent volume of control supernatant collected 16 h after UV irradiation of Huh7.5 cells transfected with HCV subgenomic replicon at 30 mJ/cm 2 prepared in the same way as the viral stock (Sg-replicon, UV). pDCs were also primed with HCV virus particles (100 HCV genomes per cell) prepared from five different sera of chronically infected patients (HCV + serum) or from equivalent volumes of four different sera of healthy individuals (HCV − serum). Two hours later, primed or mock-primed pDCs were stimulated (A) with TLR9-agonists, with CpG-A (2.5 µg/ml), or with HHV-1 KOS (multiplicity of infection = 100), or (C) with TLR7-agonists, with resiquimod (R848, 0.5-µM), or with influenza virus A/H3N2/Johannesburg (multiplicity of infection = 100). Secretion of IFN-α (A, C) or TNF-α (B) in cell-free supernatant of pDCs was determined by means of ELISA analysis 1 day post-stimulation. The results are expressed as percentages of IFN-α production from pDCs that were first primed as specified above and then further treated with the respective TLR agonist relative to IFN-α production from pDCs stimulated only with the respective TLR agonist. p W , Wilcoxon matched pairs test used to compare differences between the distributions of IFN-α production in primed and non-primed pDC-cultures; p M-W , Mann-Whitney two-tailed non-parametric test used to compare differences between the distributions of IFN-α production in HCV-exposed and Sg-replicon-exposed pDC cultures, or in HCV + serum-exposed and HCV − serum-exposed pDC cultures.

    Article Snippet: We quantified and genotyped HCV RNA from each serum sample using a branched DNA assay (Quantiplex HCV RNA 2.0 assay; Chiron Diagnostics) and a line probe assay (Inno-LiPA HCVII; Innogenetics), respectively.

    Techniques: Purification, Derivative Assay, Incubation, Irradiation, Transfection, Infection, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY, Two Tailed Test

    Kinetics of disruption of CpG-A-mediated stimulation of pDCs with HCVcc. (A) Flow chart protocol showing inoculation with HCV (solid arrows), treatment with CpG-A (dashed arrows), and IFN-α assay determined by ELISA. (B) Percentage of IFN-α secreted by pDCs that were stimulated with CpG-A and HCV relative to IFN-α secretion by pDCs stimulated only with CpG-A. Purified pDCs were inoculated with 100 HCVcc RNA copies per cell. (C) Effect of HCVcc on the expression of IFN-α, IRF-7, TLR7 and TLR9 mRNA. pDCs were primed with HCVcc and stimulated with CpG-A as shown in panel A, line a . The gene expression levels were determined with real-time PCR were normalized to GAPDH expression. Data are presented as fold induction over medium control at time zero (given the value of 1.0) and are from one of three representative experiments.

    Journal: PLoS ONE

    Article Title: Hepatitis C Virus Is a Weak Inducer of Interferon Alpha in Plasmacytoid Dendritic Cells in Comparison with Influenza and Human Herpesvirus Type-1

    doi: 10.1371/journal.pone.0004319

    Figure Lengend Snippet: Kinetics of disruption of CpG-A-mediated stimulation of pDCs with HCVcc. (A) Flow chart protocol showing inoculation with HCV (solid arrows), treatment with CpG-A (dashed arrows), and IFN-α assay determined by ELISA. (B) Percentage of IFN-α secreted by pDCs that were stimulated with CpG-A and HCV relative to IFN-α secretion by pDCs stimulated only with CpG-A. Purified pDCs were inoculated with 100 HCVcc RNA copies per cell. (C) Effect of HCVcc on the expression of IFN-α, IRF-7, TLR7 and TLR9 mRNA. pDCs were primed with HCVcc and stimulated with CpG-A as shown in panel A, line a . The gene expression levels were determined with real-time PCR were normalized to GAPDH expression. Data are presented as fold induction over medium control at time zero (given the value of 1.0) and are from one of three representative experiments.

    Article Snippet: We quantified and genotyped HCV RNA from each serum sample using a branched DNA assay (Quantiplex HCV RNA 2.0 assay; Chiron Diagnostics) and a line probe assay (Inno-LiPA HCVII; Innogenetics), respectively.

    Techniques: Flow Cytometry, Enzyme-linked Immunosorbent Assay, Purification, Expressing, Real-time Polymerase Chain Reaction

    Secretion of IFN-α induced with cell culture-derived HCVcc and patient-derived HCV in pDCs from different normal healthy donors. Purified pDCs were inoculated with different quantities of HCVcc (genotype 2) or patient-derived HCV (genotypes 1a, 1b, 2a, and 3a). Viral genomes were quantified by semiquantitative RT-PCR. As negative control, a suspension prepared from cell-free supernatant of Huh7.5 cells transfected with HCV subgenomic (sg) replicon was used. This negative control suspension was concentrated and purified in the same manner as the viral suspension used for exposure of pDCs to 100 genome-containing virus particles per cell. Resiquimod (R848, 0.5 µM) was used as a positive control. Cell cultures of pDCs purified from different normal healthy donors adjusted to a concentration of 10 6 cells/ml in the presence of IL-3 were inoculated with HCV (quantified by HCV RNA copies) in a total volume of 200 µl. Secretion of IFN-α in cell-free supernatant was determined by ELISA 1 day post-stimulation. Identical symbols at a given multiplicity of infection indicate results with pDCs of different donors.

    Journal: PLoS ONE

    Article Title: Hepatitis C Virus Is a Weak Inducer of Interferon Alpha in Plasmacytoid Dendritic Cells in Comparison with Influenza and Human Herpesvirus Type-1

    doi: 10.1371/journal.pone.0004319

    Figure Lengend Snippet: Secretion of IFN-α induced with cell culture-derived HCVcc and patient-derived HCV in pDCs from different normal healthy donors. Purified pDCs were inoculated with different quantities of HCVcc (genotype 2) or patient-derived HCV (genotypes 1a, 1b, 2a, and 3a). Viral genomes were quantified by semiquantitative RT-PCR. As negative control, a suspension prepared from cell-free supernatant of Huh7.5 cells transfected with HCV subgenomic (sg) replicon was used. This negative control suspension was concentrated and purified in the same manner as the viral suspension used for exposure of pDCs to 100 genome-containing virus particles per cell. Resiquimod (R848, 0.5 µM) was used as a positive control. Cell cultures of pDCs purified from different normal healthy donors adjusted to a concentration of 10 6 cells/ml in the presence of IL-3 were inoculated with HCV (quantified by HCV RNA copies) in a total volume of 200 µl. Secretion of IFN-α in cell-free supernatant was determined by ELISA 1 day post-stimulation. Identical symbols at a given multiplicity of infection indicate results with pDCs of different donors.

    Article Snippet: We quantified and genotyped HCV RNA from each serum sample using a branched DNA assay (Quantiplex HCV RNA 2.0 assay; Chiron Diagnostics) and a line probe assay (Inno-LiPA HCVII; Innogenetics), respectively.

    Techniques: Cell Culture, Derivative Assay, Purification, Reverse Transcription Polymerase Chain Reaction, Negative Control, Transfection, Positive Control, Concentration Assay, Enzyme-linked Immunosorbent Assay, Infection

    Liver stiffness values in HIV-monoinfected patients and in HIV/HCV patients according to plasma HIV RNA detectability or undetectability in the 12 months or 36 months before transient elastography LS, liver stiffness; kPa, kilopascal; pHIV, plasma HIV RNA; m, months .

    Journal: Annals of Gastroenterology

    Article Title: Liver stiffness is not associated with short- and long-term plasma HIV RNA replication in immunocompetent patients with HIV infection and with HIV/HCV coinfection

    doi: 10.20524/aog.2017.0175

    Figure Lengend Snippet: Liver stiffness values in HIV-monoinfected patients and in HIV/HCV patients according to plasma HIV RNA detectability or undetectability in the 12 months or 36 months before transient elastography LS, liver stiffness; kPa, kilopascal; pHIV, plasma HIV RNA; m, months .

    Article Snippet: HCV RNA genotypes were determined using the VERSANT® HCV genotype 2.0 assay (INNOLiPA, Innogenetics, Belgium).

    Techniques:

    Detection of anti-HCV antibodies in HCV RNA and antibody positive human sera with recombinant HCV proteins . 1 μg of each baculovirus-expressed and preparative SDS-PAGE-purified recombinant HCV protein was loaded onto 10–20% Tris-glycine polyacrylamide gradient gels. Core, NS2, NS3, NS4A, NS4B, and NS5A were loaded on one gel, and E1, E2, and NS5B on another gel, respectively. 3 μg of Sf 9 cell extract was also loaded onto one gel as a control. Proteins separated on gels were transferred to nylon membranes, sliced and stained with serially diluted human serum obtained from HCV RNA and antibody positive patients. The following dilutions were used (lane 1) 1:100, (lane 2) 1:500, (lane 3) 1:2500, (lane 4) 1:12500 and 1:62500 (not shown). After incubation with secondary Abs, the bands were visualized by 3-amino-9-ethylcarbazole (AEC). A. An example of highly positive human serum number 36 is shown, B. an example of a weakly positive human serum number 17 is shown.

    Journal: Virology Journal

    Article Title: Hepatitis C virus core, NS3, NS4B and NS5A are the major immunogenic proteins in humoral immunity in chronic HCV infection

    doi: 10.1186/1743-422X-6-84

    Figure Lengend Snippet: Detection of anti-HCV antibodies in HCV RNA and antibody positive human sera with recombinant HCV proteins . 1 μg of each baculovirus-expressed and preparative SDS-PAGE-purified recombinant HCV protein was loaded onto 10–20% Tris-glycine polyacrylamide gradient gels. Core, NS2, NS3, NS4A, NS4B, and NS5A were loaded on one gel, and E1, E2, and NS5B on another gel, respectively. 3 μg of Sf 9 cell extract was also loaded onto one gel as a control. Proteins separated on gels were transferred to nylon membranes, sliced and stained with serially diluted human serum obtained from HCV RNA and antibody positive patients. The following dilutions were used (lane 1) 1:100, (lane 2) 1:500, (lane 3) 1:2500, (lane 4) 1:12500 and 1:62500 (not shown). After incubation with secondary Abs, the bands were visualized by 3-amino-9-ethylcarbazole (AEC). A. An example of highly positive human serum number 36 is shown, B. an example of a weakly positive human serum number 17 is shown.

    Article Snippet: These HCV RNA and antibody positive and HCV antibody negative human serum samples were also analysed with INNO-LIA™ * HCV Ab III update or INNO-LIA™ * HCV Score test according to the manufacturer's instructions (Innogenetics, Ghent, Belgium).

    Techniques: Recombinant, SDS Page, Purification, Staining, Incubation

    The persistence of anti-HCV antibody responses against individual HCV proteins . HCV antibody prevalence in five HCV RNA and antibody positive individuals infected with genotype 1b or 3a was analyzed from serum specimens obtained before and after IFN-α monotherapy (black bar). Relative anti-HCV antibody titers were determined by Western blot analysis as described in Fig. 2.

    Journal: Virology Journal

    Article Title: Hepatitis C virus core, NS3, NS4B and NS5A are the major immunogenic proteins in humoral immunity in chronic HCV infection

    doi: 10.1186/1743-422X-6-84

    Figure Lengend Snippet: The persistence of anti-HCV antibody responses against individual HCV proteins . HCV antibody prevalence in five HCV RNA and antibody positive individuals infected with genotype 1b or 3a was analyzed from serum specimens obtained before and after IFN-α monotherapy (black bar). Relative anti-HCV antibody titers were determined by Western blot analysis as described in Fig. 2.

    Article Snippet: These HCV RNA and antibody positive and HCV antibody negative human serum samples were also analysed with INNO-LIA™ * HCV Ab III update or INNO-LIA™ * HCV Score test according to the manufacturer's instructions (Innogenetics, Ghent, Belgium).

    Techniques: Infection, Western Blot

    The specificity of anti-HCV antibody responses in patients suffering from chronic HCV infection . A. The frequency of antibodies against individual recombinant HCV proteins in 68 serum specimens obtained from patients suffering from chronic HCV infection. Both the number and percentage of positive sera are shown. B. The relative antibody levels against individual HCV proteins were determined as the last serum dilution showing a positive signal in Western blot analysis. The means and standard deviations of the means for antibody levels against individual HCV proteins are shown based on 68 HCV RNA and antibody positive patient sera. Only individuals showing a positive antibody response against a given HCV protein are included into the means.

    Journal: Virology Journal

    Article Title: Hepatitis C virus core, NS3, NS4B and NS5A are the major immunogenic proteins in humoral immunity in chronic HCV infection

    doi: 10.1186/1743-422X-6-84

    Figure Lengend Snippet: The specificity of anti-HCV antibody responses in patients suffering from chronic HCV infection . A. The frequency of antibodies against individual recombinant HCV proteins in 68 serum specimens obtained from patients suffering from chronic HCV infection. Both the number and percentage of positive sera are shown. B. The relative antibody levels against individual HCV proteins were determined as the last serum dilution showing a positive signal in Western blot analysis. The means and standard deviations of the means for antibody levels against individual HCV proteins are shown based on 68 HCV RNA and antibody positive patient sera. Only individuals showing a positive antibody response against a given HCV protein are included into the means.

    Article Snippet: These HCV RNA and antibody positive and HCV antibody negative human serum samples were also analysed with INNO-LIA™ * HCV Ab III update or INNO-LIA™ * HCV Score test according to the manufacturer's instructions (Innogenetics, Ghent, Belgium).

    Techniques: Infection, Recombinant, Western Blot