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SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + <t>CD25</t> + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.
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SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + <t>CD25</t> + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.
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SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + <t>CD25</t> + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.
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SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + <t>CD25</t> + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.
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SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + <t>CD25</t> + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.
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SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + <t>CD25</t> + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.
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SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + <t>CD25</t> + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.
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SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + <t>CD25</t> + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.
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SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + <t>CD25</t> + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.
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SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + CD25 + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.

Journal: Cell Reports Medicine

Article Title: Delayed viral rebound post-ART interruption in infant macaques given SIV-specific neutralizing antibodies

doi: 10.1016/j.xcrm.2026.102636

Figure Lengend Snippet: SIV-specific T cell responses and correlation with viral rebound AUC (A) SIVgag-specific CD8 + T cell responses were quantified by AIM assay, using Boolean gating to show the frequencies of CD69 + CD25 + , CD69 + OX40 + , or CD25 + OX40 + cells following stimulation with an SIVgag peptide pool after background subtraction. The pre-ATI (and pre-RhmAb for that group) time point was compared to the rebound peak post-ATI. Nonparametric Wilcoxon matched-pairs signed rank test was used for statistics. N = 4 and N = 5 for controls at each time point based on sample availability. (B) Graph shows the frequency of SIVgag-specific CD8 + T cells at peak rebound in the RhmAb group and rebound viral load AUC. Statistical analysis was performed by calculating the nonparametric Spearman’s rank correlation coefficient (r) that was compared to zero.

Article Snippet: PE-Vio770 Mouse Anti-Human CD25 , Miltenyi Biotec , 130-113-287; RRID:AB_2784092.

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