ABSTRACT
The emergence of 2019 novel coronavirus disease (COVID-19) is currently a global concern. In this study, our goal was to explore the changing expression levels of acute-phase reaction proteins (APRPs) in the serum of COVID-19 patients and to elucidate the immunological characteristics of COVID-19. In the study design, we recruited 72 COVID-19 patients, including 22 cases of mild degree, 38 cases of moderate degree and 12 cases of severe degree. We also recruited 20 patients with community-acquired pneumonia (CAP) and 20 normal control subjects as a comparison. Fasting venous blood was taken to detect the content of complement 3 (C3), complement 4 (C4), C-reactive protein (CRP), serum amyloid A (SAA) and prealbumin (PA). When compared the COVID-19 group with the CAP and normal control groups, respectively, the mean value of CRP and SAA in the COVID-19 group (including mild, moderate and severe patients) had increased significantly (P < 0.01), whereas the mean values of C3, C4 and PA decreased (P < 0.01). For the asymptomatic or mild symptomatic patients with COVID-19, the actual aggravation of disease may be more advanced than the clinical appearances. Meanwhile, the statistical analyses indicated that the development of COVID-19 brought about a significant increase in the content of CRP and SAA (P < 0.01), and a decline in the content of C3, C4 and PA (P < 0.01). These findings suggested that the changes in the level of APRPs could be used as indicators to identify the degree and progression of COVID-19, and the significant changes might demonstrate the aggravation of disease. This study provided a new approach to improve the clinical management plan and prognosis of COVID-19.
Subject(s)
Acute-Phase Proteins/analysis , Acute-Phase Proteins/biosynthesis , Coronavirus Infections/diagnosis , Coronavirus Infections/therapy , Pneumonia, Viral/diagnosis , Pneumonia, Viral/therapy , Adult , Aged , C-Reactive Protein/analysis , C-Reactive Protein/biosynthesis , COVID-19 , Case-Control Studies , Community-Acquired Infections/blood , Community-Acquired Infections/immunology , Complement C3/analysis , Complement C3/biosynthesis , Complement C4/analysis , Complement C4/biosynthesis , Coronavirus Infections/blood , Coronavirus Infections/immunology , Female , Humans , Male , Middle Aged , Pandemics , Pneumonia/blood , Pneumonia/immunology , Pneumonia, Viral/blood , Pneumonia, Viral/immunology , Prealbumin/analysis , Prealbumin/biosynthesis , Prognosis , Serum Amyloid A Protein/analysis , Serum Amyloid A Protein/biosynthesis , Severity of Illness Index , Young AdultSubject(s)
Antigen-Antibody Complex/biosynthesis , Betacoronavirus/pathogenicity , Coronavirus Infections/immunology , Cytokine Release Syndrome/immunology , Immune Complex Diseases/immunology , Pneumonia, Viral/immunology , Severe Acute Respiratory Syndrome/immunology , Vasculitis/immunology , Antibodies, Viral/biosynthesis , Antigen-Antibody Complex/drug effects , Betacoronavirus/immunology , Blood Vessels/drug effects , Blood Vessels/immunology , Blood Vessels/pathology , Blood Vessels/virology , COVID-19 , Complement C3/antagonists & inhibitors , Complement C3/biosynthesis , Complement Inactivating Agents/therapeutic use , Coronavirus Infections/complications , Coronavirus Infections/drug therapy , Coronavirus Infections/virology , Cytokine Release Syndrome/complications , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/virology , Humans , Immune Complex Diseases/complications , Immune Complex Diseases/drug therapy , Immune Complex Diseases/virology , Immunity, Humoral/drug effects , Interleukin 1 Receptor Antagonist Protein/therapeutic use , Interleukin-6/antagonists & inhibitors , Interleukin-6/biosynthesis , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/drug therapy , Pneumonia, Viral/virology , Receptors, Interleukin-1/antagonists & inhibitors , Receptors, Interleukin-1/biosynthesis , SARS-CoV-2 , Severe Acute Respiratory Syndrome/complications , Severe Acute Respiratory Syndrome/drug therapy , Severe Acute Respiratory Syndrome/virology , Severity of Illness Index , Vasculitis/complications , Vasculitis/drug therapy , Vasculitis/virologyABSTRACT
Coronavirus Disease 2019 (COVID-19) is an ongoing public health emergency and new knowledge about its immunopathogenic mechanisms is deemed necessary in the attempt to reduce the death burden, globally. For the first time in worldwide literature, we provide scientific evidence that in COVID-19 vasculitis a life-threatening escalation from type 2 T-helper immune response (humoral immunity) to type 3 hypersensitivity (immune complex disease) takes place. The subsequent deposition of immune complexes inside the vascular walls is supposed to induce a severe inflammatory state and a cytokine release syndrome, whose interleukin-6 is the key myokine, from the smooth muscle cells of blood vessels.