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95
ATCC hrv a16
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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TaKaRa hrv 3c protease
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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Firstbeat Technologies Ltd life (hrv & movement measurement based wellbeing service
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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TaKaRa gst cas9sv40
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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TaKaRa human rhinovirus hrv 3c protease
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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ADInstruments hrv module
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.
Hrv Module, supplied by ADInstruments, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
Addgene inc marcel bruchez
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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Addgene inc plasmid pet2110xhis gst hrv her2 dl5 her2
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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ATCC hrv a19
(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