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Abstract
Since its emergence at the end of 2019, SARS-CoV-2 has spread worldwide at a very rapid pace. While most infected individuals have an asymptomatic or mild disease, a minority, mainly the elderly, develop a severe disease that may lead to a fatal acute respiratory distress syndrome (ARDS). ARDS results from a highly inflammatory immunopathology process that includes systemic manifestations and massive alveolar damages that impair gas exchange. The present review summarizes our current knowledge in the rapidly evolving field of SARS-CoV-2 immunopathology, emphasizing the role of specific T cell responses. Indeed, accumulating evidence suggest that while T-cell response directed against SARS-CoV-2 likely plays a crucial role in virus clearance, it may also participate in the immunopathology process that leads to ARDS.
Highlights
Coronaviruses are a family of single-strand positive RNA enveloped viruses that infect a wide range of hosts
The highly inflammatory process leading to acute respiratory distress syndrome (ARDS) results from inappropriate regulation of the network of innate and adaptive components of the immune response triggered by SARS-CoV-2 replication in the pulmonary alveolus
The anti-SARS-CoV-2 primary T cell response, which includes the complex and multifaceted CD4 T cell response and the CD8 T cell component, likely plays an essential role in virus clearance. It may participate in the immunopathology process leading to ARDS
Summary
Coronaviruses are a family of single-strand positive RNA enveloped viruses that infect a wide range of hosts. Seven viruses are known to infect humans They include four common human coronaviruses: 229E and NL63 (alpha coronavirus) and OC43 and HKU1 (beta coronavirus). The highly contagious SARS-CoV-2, which outbreak started in the province of Wuhan in China at the end of 2019, and which spread worldwide at a very rapid pace Those three highly pathogenic coronaviruses predominantly infect the lower respiratory tract, mainly alveolar epithelial cells. In SARS-CoV-2 infected patients, ARDS occurs approximately between day 9 and day 12 following the onset of symptoms [11] It is associated with biological hallmarks of intense inflammation (e.g., increase of serum ferritin and CRP), coagulation activation (e.g., increase of d-dimers), and heart damage (e.g., increase of Troponin). The incidence of thrombotic complications appears high in intensive care unit patients with SARS-CoV-2, with pulmonary embolism being the most frequent, ranging from 20.6 to 31% [12, 13]
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