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hrv module  (ADInstruments)


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    ADInstruments hrv module
    Hrv Module, supplied by ADInstruments, used in various techniques. Bioz Stars score: 95/100, based on 172 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hrv module/product/ADInstruments
    Average 95 stars, based on 172 article reviews
    hrv module - by Bioz Stars, 2026-05
    95/100 stars

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    A. Schematic representation of the infection experiment to assess the ability of aptamers to block rhinovirus infection. Aptamers (I4, I5 and I8) were tested at doses of 1 and 0.1 µM. As positive control, for assessing viral inhibition, a VP1 inhibitor (Pleconaril, pleco) was also included. H1-HeLa cells were pre-treated with aptamers for 7 minutes and next the infection <t>with</t> <t>HRV-A16</t> (MOI 0.1) was performed. After 1 hours, the inoculum was removed and infection was allowed to proceed for 72 hours at 33°C. Infectious virus released into the supernatant was quantified by TCID₅₀ assay (B), and viral RNA levels were measured (C). B. Normalized viral titers (%), expressed relative to vehicle (100%) and mock (0%) (mean ± SEM). C. Viral RNA levels assessed by RT-PCR using HRV-specific primers. Data are shown as 2 -ΔCt . Statistical significance was determined by ordinary one-way ANOVA followed by Bonferroni’s multiple comparison correction vs vehicle.
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    A. Schematic representation of the infection experiment to assess the ability of aptamers to block rhinovirus infection. Aptamers (I4, I5 and I8) were tested at doses of 1 and 0.1 µM. As positive control, for assessing viral inhibition, a VP1 inhibitor (Pleconaril, pleco) was also included. H1-HeLa cells were pre-treated with aptamers for 7 minutes and next the infection <t>with</t> <t>HRV-A16</t> (MOI 0.1) was performed. After 1 hours, the inoculum was removed and infection was allowed to proceed for 72 hours at 33°C. Infectious virus released into the supernatant was quantified by TCID₅₀ assay (B), and viral RNA levels were measured (C). B. Normalized viral titers (%), expressed relative to vehicle (100%) and mock (0%) (mean ± SEM). C. Viral RNA levels assessed by RT-PCR using HRV-specific primers. Data are shown as 2 -ΔCt . Statistical significance was determined by ordinary one-way ANOVA followed by Bonferroni’s multiple comparison correction vs vehicle.
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    A. Schematic representation of the infection experiment to assess the ability of aptamers to block rhinovirus infection. Aptamers (I4, I5 and I8) were tested at doses of 1 and 0.1 µM. As positive control, for assessing viral inhibition, a VP1 inhibitor (Pleconaril, pleco) was also included. H1-HeLa cells were pre-treated with aptamers for 7 minutes and next the infection <t>with</t> <t>HRV-A16</t> (MOI 0.1) was performed. After 1 hours, the inoculum was removed and infection was allowed to proceed for 72 hours at 33°C. Infectious virus released into the supernatant was quantified by TCID₅₀ assay (B), and viral RNA levels were measured (C). B. Normalized viral titers (%), expressed relative to vehicle (100%) and mock (0%) (mean ± SEM). C. Viral RNA levels assessed by RT-PCR using HRV-specific primers. Data are shown as 2 -ΔCt . Statistical significance was determined by ordinary one-way ANOVA followed by Bonferroni’s multiple comparison correction vs vehicle.
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    A. Schematic representation of the infection experiment to assess the ability of aptamers to block rhinovirus infection. Aptamers (I4, I5 and I8) were tested at doses of 1 and 0.1 µM. As positive control, for assessing viral inhibition, a VP1 inhibitor (Pleconaril, pleco) was also included. H1-HeLa cells were pre-treated with aptamers for 7 minutes and next the infection <t>with</t> <t>HRV-A16</t> (MOI 0.1) was performed. After 1 hours, the inoculum was removed and infection was allowed to proceed for 72 hours at 33°C. Infectious virus released into the supernatant was quantified by TCID₅₀ assay (B), and viral RNA levels were measured (C). B. Normalized viral titers (%), expressed relative to vehicle (100%) and mock (0%) (mean ± SEM). C. Viral RNA levels assessed by RT-PCR using HRV-specific primers. Data are shown as 2 -ΔCt . Statistical significance was determined by ordinary one-way ANOVA followed by Bonferroni’s multiple comparison correction vs vehicle.
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    A. Schematic representation of the infection experiment to assess the ability of aptamers to block rhinovirus infection. Aptamers (I4, I5 and I8) were tested at doses of 1 and 0.1 µM. As positive control, for assessing viral inhibition, a VP1 inhibitor (Pleconaril, pleco) was also included. H1-HeLa cells were pre-treated with aptamers for 7 minutes and next the infection <t>with</t> <t>HRV-A16</t> (MOI 0.1) was performed. After 1 hours, the inoculum was removed and infection was allowed to proceed for 72 hours at 33°C. Infectious virus released into the supernatant was quantified by TCID₅₀ assay (B), and viral RNA levels were measured (C). B. Normalized viral titers (%), expressed relative to vehicle (100%) and mock (0%) (mean ± SEM). C. Viral RNA levels assessed by RT-PCR using HRV-specific primers. Data are shown as 2 -ΔCt . Statistical significance was determined by ordinary one-way ANOVA followed by Bonferroni’s multiple comparison correction vs vehicle.
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    (A) Amino acid (AA) variation in the historical HRV-A genome. The bottom panel shows AA differences across the CDS between the historical HRV A and any HRV <t>A19</t> (green lines) and AA positions that are unique to the historical HRV A relative to all HRV A sequences (purple lines). Green line height indicates the proportion of HRV A19 sequences differing at each position. Historical HRV A genome coverage is shown in the background, with coding sequence annotations below. The top panel shows Shannon entropy per AA position (blue). Purple arrows mark the two historical-specific AAs with near-zero entropy (∼0.01). Dashed and dotted red lines denote highly (>2) and moderately (>1) variable positions, respectively. ( B) BETS analyses displaying the log Bayes Factor (Δ MLE ) from BEAST trees including tip dates (heterochronous) and those not including tip dates (isochronous). The Marginal Likelihood Estimates are calculated from BEAST trees utilizing a Generalized Stepping-Stone Sampling analyses. A Δ MLE greater than 3 is sufficient to assume strong temporal signal(44). The 95% HPD of the mean substitution rate and root age are annotated in brackets. ( C) Time-calibrated maximum clade credibility (MCC) BEAST tree under a strict molecular clock and coalescent constant population prior utilizing full-genome sequences of genotypes A22, A82, A94 and A19 (indicated in color). The 95% HPD of each node is shown by the blue horizontal bars and the posteriors for each node are displayed as a number, 0-1. Estimated time (years) is displayed on the x-axis.
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    A. Schematic representation of the infection experiment to assess the ability of aptamers to block rhinovirus infection. Aptamers (I4, I5 and I8) were tested at doses of 1 and 0.1 µM. As positive control, for assessing viral inhibition, a VP1 inhibitor (Pleconaril, pleco) was also included. H1-HeLa cells were pre-treated with aptamers for 7 minutes and next the infection with HRV-A16 (MOI 0.1) was performed. After 1 hours, the inoculum was removed and infection was allowed to proceed for 72 hours at 33°C. Infectious virus released into the supernatant was quantified by TCID₅₀ assay (B), and viral RNA levels were measured (C). B. Normalized viral titers (%), expressed relative to vehicle (100%) and mock (0%) (mean ± SEM). C. Viral RNA levels assessed by RT-PCR using HRV-specific primers. Data are shown as 2 -ΔCt . Statistical significance was determined by ordinary one-way ANOVA followed by Bonferroni’s multiple comparison correction vs vehicle.

    Journal: bioRxiv

    Article Title: Identification of ICAM-1–targeting DNA aptamers as a host-directed strategy to inhibit Human Rhinovirus infection

    doi: 10.64898/2026.04.20.717810

    Figure Lengend Snippet: A. Schematic representation of the infection experiment to assess the ability of aptamers to block rhinovirus infection. Aptamers (I4, I5 and I8) were tested at doses of 1 and 0.1 µM. As positive control, for assessing viral inhibition, a VP1 inhibitor (Pleconaril, pleco) was also included. H1-HeLa cells were pre-treated with aptamers for 7 minutes and next the infection with HRV-A16 (MOI 0.1) was performed. After 1 hours, the inoculum was removed and infection was allowed to proceed for 72 hours at 33°C. Infectious virus released into the supernatant was quantified by TCID₅₀ assay (B), and viral RNA levels were measured (C). B. Normalized viral titers (%), expressed relative to vehicle (100%) and mock (0%) (mean ± SEM). C. Viral RNA levels assessed by RT-PCR using HRV-specific primers. Data are shown as 2 -ΔCt . Statistical significance was determined by ordinary one-way ANOVA followed by Bonferroni’s multiple comparison correction vs vehicle.

    Article Snippet: HRV-A16 (Human Rhinovirus A 16) strain 11757 was purchased from ATCC (LGC, Italy, cat. n°: VR-283).

    Techniques: Infection, Blocking Assay, Positive Control, Inhibition, Virus, Reverse Transcription Polymerase Chain Reaction, Comparison

    (A) Amino acid (AA) variation in the historical HRV-A genome. The bottom panel shows AA differences across the CDS between the historical HRV A and any HRV A19 (green lines) and AA positions that are unique to the historical HRV A relative to all HRV A sequences (purple lines). Green line height indicates the proportion of HRV A19 sequences differing at each position. Historical HRV A genome coverage is shown in the background, with coding sequence annotations below. The top panel shows Shannon entropy per AA position (blue). Purple arrows mark the two historical-specific AAs with near-zero entropy (∼0.01). Dashed and dotted red lines denote highly (>2) and moderately (>1) variable positions, respectively. ( B) BETS analyses displaying the log Bayes Factor (Δ MLE ) from BEAST trees including tip dates (heterochronous) and those not including tip dates (isochronous). The Marginal Likelihood Estimates are calculated from BEAST trees utilizing a Generalized Stepping-Stone Sampling analyses. A Δ MLE greater than 3 is sufficient to assume strong temporal signal(44). The 95% HPD of the mean substitution rate and root age are annotated in brackets. ( C) Time-calibrated maximum clade credibility (MCC) BEAST tree under a strict molecular clock and coalescent constant population prior utilizing full-genome sequences of genotypes A22, A82, A94 and A19 (indicated in color). The 95% HPD of each node is shown by the blue horizontal bars and the posteriors for each node are displayed as a number, 0-1. Estimated time (years) is displayed on the x-axis.

    Journal: bioRxiv

    Article Title: Recovery of an 18 th Century Rhinovirus Genome through Ancient RNA Isolation of Human Lungs

    doi: 10.64898/2026.01.29.702071

    Figure Lengend Snippet: (A) Amino acid (AA) variation in the historical HRV-A genome. The bottom panel shows AA differences across the CDS between the historical HRV A and any HRV A19 (green lines) and AA positions that are unique to the historical HRV A relative to all HRV A sequences (purple lines). Green line height indicates the proportion of HRV A19 sequences differing at each position. Historical HRV A genome coverage is shown in the background, with coding sequence annotations below. The top panel shows Shannon entropy per AA position (blue). Purple arrows mark the two historical-specific AAs with near-zero entropy (∼0.01). Dashed and dotted red lines denote highly (>2) and moderately (>1) variable positions, respectively. ( B) BETS analyses displaying the log Bayes Factor (Δ MLE ) from BEAST trees including tip dates (heterochronous) and those not including tip dates (isochronous). The Marginal Likelihood Estimates are calculated from BEAST trees utilizing a Generalized Stepping-Stone Sampling analyses. A Δ MLE greater than 3 is sufficient to assume strong temporal signal(44). The 95% HPD of the mean substitution rate and root age are annotated in brackets. ( C) Time-calibrated maximum clade credibility (MCC) BEAST tree under a strict molecular clock and coalescent constant population prior utilizing full-genome sequences of genotypes A22, A82, A94 and A19 (indicated in color). The 95% HPD of each node is shown by the blue horizontal bars and the posteriors for each node are displayed as a number, 0-1. Estimated time (years) is displayed on the x-axis.

    Article Snippet: We observed that the coding sequence (CDS) of the historical HRV A genome has the highest nucleotide (86.24%) and amino acid (93.8%) identity to the ATCC reference sequence of HRV A19 (accession: FJ445119.1 ).

    Techniques: Sequencing, Sampling