We next asked whether these T and B cell dynamics related to clinical measures of COVID-19 disease, by correlating changes in immune features from D0 to D7 with clinical information (Fig. 5G). These analyses revealed distinct correlations. Decreases in all populations of responding CD4 and CD8 T cells (HLA-DR+CD38+, KI67+, or activated cTfh) between D0 and D7 were positively correlated with PMN and WBC counts, suggesting a relationship between T cell activation and lymphopenia. Furthermore, decreases in CD4 and CD8 HLA-DR+CD38+ T cells positively correlated with APACHE III score. However, stable HLA-DR+CD38+ CD4 T cell responses correlated with coagulation complications and ferritin. Whereas decreasing activated cTfh over time was related to co-infection, the opposite pattern was observed for PB. Increases in proliferating KI67+ CD4 and CD8 T cells over time were positively correlated to increasing anti-SARS-CoV2 antibody from day 0 to day 7, suggesting that some individuals might have been hospitalized during the expansion phase of the antiviral immune response (Fig. 5G). Finally, neither Remdesivir nor HCQ treatment correlated with any of these immune features in Fig. 5G). Examining categorical rather than continuous clinical data, 80% of patients with decreasing PB over time had hyperlipidemia, whereas only 20% of patients with increasing PB over time had this comorbidity (fig. S6D). All patients who had decreasing CD38+HLA-DR+ CD8 T cells from day 0 to day 7 were treated with early vasoactive medication or inhaled nitric oxide whereas these treatments were less common for patients with stable or increasing CD38+HLA-DR+ CD8 T cells (fig. S6E). In contrast, vasoactive medication, inhaled nitric oxide, and early steroid treatment were equally common in patients with increasing or decreasing PB (fig. S6D). Similar patterns were apparent for other T cell populations and these categorical clinical data (fig. S6F). Thus, the trajectory of change in the T and B cell response in COVID-19 patients was strongly connected to clinical metrics of disease.