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Fig. 3 | Journal of Translational Medicine

Fig. 3

From: Pathophysiology and treatment strategies for COVID-19

Fig. 3

An infection and replication model of SARS-CoV-2 in host cells and current treatment strategies to interfere with steps in the SARS-CoV-2 replication cycle. SARS-CoV-2 binds to host cells through the ACE2 receptor, and after endocytosis and subsequent uncoating, the components of SARS-CoV-2 use host cells machinery to produce new viruses. Finally, the SARS-CoV-2 virions are released from the host cell by exocytosis. During this process, the viral replication can be inhibited at different stages by repositioned drugs (highlighted in red). On the other hand, SARS-CoV-2 stimulates the host immune system to release the cytokines and subsequent inflammation and immune-dysfunction through activation or impairment of various immune cells, such, dendritic cells, NK cells, macrophages, and neutrophils. This process can lead to sepsis, septic shock, multiple organ failure, and death. SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; TMPRSS2, transmembrane protease serine 2; NK, natural killer; DC, dendritic cell; IL-1, interleukin-1; IL-6, interleukin-6

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