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Viral infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) lead to the development of coronavirus disease 2019 (COVID-19), and while many infected individuals fail to develop noticeable symptoms and others develop mild to moderate symptoms, a significant proportion develop severe or critical symptoms (with the latter including respiratory failure, shock, or multiorgan dysfunction) that can end in patient death. SARS-CoV-2 predominantly infects cells of the respiratory system,1 employing the angiotensin-converting enzyme 2 (ACE2) receptor as a means of entry2; however, the expression of ACE2 in multiple cell types in multiple tissues makes them highly susceptible to SARS-CoV-2 infection, which may explain, in part, the impact on multiple organ systems in COVID-19 patients. Viral replication within infected cells prompts apoptosis and the release of pro-inflammatory cytokines,3 which can induce a cytokine storm that prompts the development of acute respiratory distress syndrome, multiorgan failure, and death.4 Beyond supportive care for severely affected patients, we generally lack adequate treatment options; furthermore, we also lack faithful model systems to explore the SARS-CoV-2 lifecycle and evaluate the efficacy of potential stem cell therapeutics. In the first of our Featured Articles published this month in Stem Cells, Djidrovski et al describe the ability of SARS-CoV-2 to infect an induced pluripotent stem cell (iPSC)-derived airway model system in a study that may pave the way for broader and reproducible studies of viral airway infection.5 In a Related Article published recently in Stem Cells Translational Medicine, Desterke et al explored the expression of the ACE2 receptor (used for SARs-CoV-2 entry) in mesenchymal stem cells (MSCs) to assess their safety and potential as anti-inflammatory therapies for severe COVID-19 patients.6

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