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Fig. 2 | Journal of Biomedical Science

Fig. 2

From: Insights to SARS-CoV-2 life cycle, pathophysiology, and rationalized treatments that target COVID-19 clinical complications

Fig. 2

Major severe COVID-19 pathologies and infection routes. a The modules involved in, 10. acute phase of SARS-CoV-2 infection in the lung (ARDS); 11. vasodilation, increased capillary permeability, apoptosis/necrosis of endothelial cells as well as 12. ARDS-induced “cytokine storm” and likely virus entry to the circulation which may then cause systemic failure due to broad organotropism in tissues expressing high levels of ACE2 (e.g., heart and kidneys) or the “cytokine storm”-related excessive inflammation, are indicated. b Sites of potentially SARS-CoV-2 infected organs in the alimentary tract of the digestive system and in accessory organs i.e., salivary glands, liver, gallbladder, and pancreas. ACE2 is expressed in relatively high levels in duodenum, small and large intestines, rectum, as well as in gallbladder. Thus, following the consumption of contaminated food the virus likely reaches the stomach passively; the reported adverse effects in other accessory organs like liver or pancreas are probably the result of excessive inflammation during severe COVID-19. c Central (brain, spinal cord) and peripheral nervous system as an infection route of SARS-CoV-2; ACE2, neuropilin-1 (NRP1) and CD147 that reportedly potentiate virus infectivity into the central nervous system are shown. The molecular pathways involved in SARS-CoV-2 infection in human (e.g., lung) cells are depicted in Fig. 1

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