Coronavirus Disease 2019: The Role of the Fibrinolytic System from Transmission to Organ Injury and Sequelae

An initial cluster of severe viral pneumonia was discovered in early December 2019 in Wuhan, China. It was found to be caused by a newly identified coronavirus, later named by the World Health Organization and the Coronavirus Study Group of the International Committee as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the disease as coronavirus disease 2019 (COVID-19).[1] [2] [3] [4] The disease rapidly spread globally and was then declared as a pandemic. The most notable characteristic of SARS-CoV-2 is its high infectivity. As a result, much attention has been paid to its mode of transmission. The major route of infection is the binding of the spike protein of the virus to its natural receptor angiotensin-converting enzyme (ACE 2) on the surface of the host cells.[2] ACE2 is present in tissues and is particularly abundantly expressed in the lung in the alveolar (type II) cells. This is clinically correlated as the lung is the major organ affected by the viral infection, leading to acute respiratory failure and acute respiratory distress syndrome (ARDS). Many aspects of COVID-19 are similar to those seen in the SARS and in the Middle East respiratory syndrome (MERS),[5] [6] including ACE2 being the receptor for the virus.[7] Impaired fibrinolysis was observed in post-SARS complications.[8] [9] Impairedfibrinolysis[10] [11] is present in pneumonia and acute lung injuries; accordingly, this commentary is devoted to reviewing evidence for possible involvement of the fibrinolytic system in transmission, pulmonary complications, and sequelae of COVID-19. Several possible drug targets that alter the activity of components of the fibrinolytic system are also discussed.

Publikationsverlauf

Artikel online veröffentlicht:
09. Mai 2020

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