Abstract
The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its rapid international spread has caused the coronavirus disease 2019 (COVID-19) pandemics, which is a global public health crisis. Thus, there is an urgent need to establish biological models to study the pathology of SARS-CoV-2 infection, which not only involves respiratory failure, but also includes dysregulation of other organs and systems, including the brain, heart, liver, intestines, pancreas, kidneys, eyes, and so on. Cellular and organoid models derived from human induced pluripotent stem cells (iPSCs) are ideal tools for in vitro simulation of viral life cycles and drug screening to prevent the reemergence of coronavirus. These iPSC-derived models could recapitulate the functions and physiology of various human cell types and assemble the complex microenvironments similar with those in the human organs; therefore, they can improve the study efficiency of viral infection mechanisms, mimic the natural host-virus interaction, and be suited for long-term experiments. In this review, we focus on the application of in vitro iPSC-derived cellular and organoid models in COVID-19 studies.
Highlights
Since its outbreak in 2019, the coronavirus disease (COVID-19) pandemics have infected more than 190 million people and caused more than 4 million deaths1
The purpose of this review is to describe the usefulness of these induced pluripotent stem cells (iPSCs)-derived cellular and organoid models in simulating human cellular physiology and tissue microenvironment, and enabling the study of hostvirus interaction and drug screening for the COVID-19 disease, leading to a more comprehensive understanding of the SARS-CoV-2 pathogenesis
Single-cell RNA-seq has been employed to screen for cell types that are positive of the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) and effector protease TMPRSS2, and to illustrate the transcriptional alternations after viral
Summary
Since its outbreak in 2019, the coronavirus disease (COVID-19) pandemics have infected more than 190 million people and caused more than 4 million deaths. COVID-19 is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), an enveloped positive-sense singlestranded RNA virus. It enters the host cells using angiotensin-converting enzyme 2 (ACE2) as the cell surface receptor and transmembrane serine protease 2 (TMPRSS2) as the effector to cleave its spike protein (Hoffmann et al, 2020). Respiratory failure is the most common cause of death in COVID-19 patients; severe fatal manifestations are observed in other organs, such as the brain, heart, liver, intestines, and pancreas (Puelles et al, 2020). It is of particular importance to find models that can imitate the natural host-virus interactions of SARSCoV-2 in a variety of human cell types and organs, improving the study efficiency for identifying key molecular regulators and the underlying mechanisms of virus infection and disease progression
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