Clinically distinct COVID-19 cases share notably similar immune response progression: A follow-up analysis

Sustained expression of inflammatory monocytes and activated T cells in COVID‐19 patients and recovered convalescent plasma donors

“…It was suggested that as SERPING1 works as in a negative feedback loop to control contact and complement system activation, the enhanced level of SERPING1 is an attempt by the host to constrain inappropriate complement activation. 23 …”

“…Besides, the increased level of SERPING1 which transcriptionally regulated by IFN‐γ was shown to be correlated with COVID‐19. It was suggested that as SERPING1 works as in a negative feedback loop to control contact and complement system activation, the enhanced level of SERPING1 is an attempt by the host to constrain inappropriate complement activation 23 …”

Targeting thromboinflammation in COVID-19 – A narrative review of the potential of C1 inhibitor to prevent disease progression

“…C1-INH activity was also elevated in hospitalized COVID-19 cancer patients compared to healthy controls ( Peerschke et al, 2021 ). In a proteomic analysis of sera, C1-INH expression was found to be significantly upregulated in severe vs. non-severe COVID-19 patients but also in COVID-19 compared to control individuals ( Hausburg et al, 2021 , Shen et al, 2020 ). Similarly, C1-INH concentration and activity was elevated in plasma but also in BALF of patients with life-threatening COVID-19 compared to healthy controls ( Nossent et al, 2021 ).…”

C1 esterase inhibitor-mediated immunosuppression in COVID-19: Friend or foe?

“…Prior to the COVID-19 pandemic, SERPING1 expression had been characterized in SARS-CoV-1 patients and found to be increased in whole blood RNA when compared to healthy controls [54] . And again, when compared to healthy controls SARS-CoV-2 infection was associated with increased SERPING1 transcript in whole blood RNA [ 9 , 54 , 55 ]. However, SERPING1 was found to be decreased in mRNA purified from bronchoalveolar lavage fluid from COVID patients when compared to a mixed cohort of subjects and controls from a previous study of obesity and asthmatic disease severity [56] .…”

“…Suppression of IFN production has been shown by the nucleocapsid proteins of both Middle East respiratory syndrome coronavirus (MERS-CoV) and SARS-CoV-1 [60] . However, the debate of whether SARS-CoV2-mediated IFN signaling is delayed/disrupted or robust has been the focus of numerous COVID-19 studies [ 3 , 8 , 9 , 59 , [61] , [62] , [63] , [64] , [65] , [66] , [67] ].…”