SARS-CoV-2, the virus underlying COVID-19, has now been recognized to cause multiorgan disease with a systemic effect on the host. To effectively combat SARS-CoV-2 and the subsequent development of COVID-19, it is critical to detect, monitor, and model viral pathogenesis. In this review, we discuss recent advancements in microfluidics, organ-on-a-chip, and human stem cell–derived models to study SARS-CoV-2 infection in the physiological organ microenvironment, together with their limitations. Microfluidic-based detection methods have greatly enhanced the rapidity, accessibility, and sensitivity of viral detection from patient samples. Engineered organ-on-a-chip models that recapitulate in vivo physiology have been developed for many organ systems to study viral pathology. Human stem cell–derived models have been utilized not only to model viral tropism and pathogenesis in a physiologically relevant context but also to screen for effective therapeutic compounds. The combination of all these platforms, along with future advancements, may aid to identify potential targets and develop novel strategies to counteract COVID-19 pathogenesis.
Although SARS-CoV-2, the causative virus of the global COVID-19 pandemic, primarily affects the respiratory tract, it is now recognized to have broad multi-organ tropism and systemic effects. Early reports indicated that SARS-CoV-2 infection could lead to cardiac damage, suggesting the virus may directly impact the heart. Cardiac cell types derived from human pluripotent stem cells (hPSCs) enable mechanistic interrogation of SARS-CoV-2 infection in human cardiac tissue. Purpose of Review To review the studies published since the emergence of the COVID-19 pandemic which utilize hPSCs and their cardiovascular derivative cell types to interrogate the tropism and effects of SARS-CoV-2 infection in the heart, as well as explore potential therapies. Recent Findings Recent studies reveal that SARS-CoV-2 is capable of infecting and replicating within hPSC-derived cardiomyocytes and sinoatrial nodal cells, but not as extensively in their non-parenchymal counterparts. Additionally, they show striking viral effects on cardiomyocyte structure, transcriptional activity, and survival, along with potential mechanisms and therapeutic targets. Summary Cardiac models derived from hPSCs are a viable platform to study the impact of SARS-CoV-2 on cardiac tissue and may lead to novel mechanistic insight as well as therapeutic interventions.
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