학술논문

Clinical and Immunological Factors That Distinguish COVID-19 From Pandemic Influenza A(H1N1)
Document Type
article
Source
Subject
Medical Microbiology
Biomedical and Clinical Sciences
Clinical Sciences
Influenza
Lung
Pneumonia & Influenza
Infectious Diseases
Prevention
Clinical Research
Biodefense
Emerging Infectious Diseases
Vaccine Related
Pneumonia
2.1 Biological and endogenous factors
Aetiology
Infection
Inflammatory and immune system
Good Health and Well Being
Adult
Aged
COVID-19
Cytokines
Female
Humans
Influenza A Virus
H1N1 Subtype
Influenza
Human
Male
Matrix Metalloproteinase 1
Matrix Metalloproteinase 3
Middle Aged
Prospective Studies
Receptors
Immunologic
Th1 Cells
Th2 Cells
SARS-CoV-2
pandemic influenza
acute respiratory distress syndrome
Influenza A(H1N1) pdm09
Immunology
Biochemistry and cell biology
Genetics
Language
Abstract
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), is a global health threat with the potential to cause severe disease manifestations in the lungs. Although COVID-19 has been extensively characterized clinically, the factors distinguishing SARS-CoV-2 from other respiratory viruses are unknown. Here, we compared the clinical, histopathological, and immunological characteristics of patients with COVID-19 and pandemic influenza A(H1N1). We observed a higher frequency of respiratory symptoms, increased tissue injury markers, and a histological pattern of alveolar pneumonia in pandemic influenza A(H1N1) patients. Conversely, dry cough, gastrointestinal symptoms and interstitial lung pathology were observed in COVID-19 cases. Pandemic influenza A(H1N1) was characterized by higher levels of IL-1RA, TNF-α, CCL3, G-CSF, APRIL, sTNF-R1, sTNF-R2, sCD30, and sCD163. Meanwhile, COVID-19 displayed an immune profile distinguished by increased Th1 (IL-12, IFN-γ) and Th2 (IL-4, IL-5, IL-10, IL-13) cytokine levels, along with IL-1β, IL-6, CCL11, VEGF, TWEAK, TSLP, MMP-1, and MMP-3. Our data suggest that SARS-CoV-2 induces a dysbalanced polyfunctional inflammatory response that is different from the immune response against pandemic influenza A(H1N1). Furthermore, we demonstrated the diagnostic potential of some clinical and immune factors to differentiate both diseases. These findings might be relevant for the ongoing and future influenza seasons in the Northern Hemisphere, which are historically unique due to their convergence with the COVID-19 pandemic.