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Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), the virus that causes coronavirus disease 2019 (COVID‐19), has led to an unprecedented public health emergency worldwide. While common cold symptoms are observed in mild cases, COVID‐19 is accompanied by multiorgan failure in severe patients. Organ damage in COVID‐19 patients is partially associated with the indirect effects of SARS‐CoV‐2 infection (e.g., systemic inflammation, hypoxic‐ischemic damage, coagulopathy), but early processes in COVID‐19 patients that trigger a chain of indirect effects are connected with the direct infection of cells by the virus. To understand the virus transmission routes and the reasons for the wide‐spectrum of complications and severe outcomes of COVID‐19, it is important to identify the cells targeted by SARS‐CoV‐2. This review summarizes the major steps of investigation and the most recent findings regarding SARS‐CoV‐2 cellular tropism and the possible connection between the early stages of infection and multiorgan failure in COVID‐19. The SARS‐CoV‐2 pandemic is the first epidemic in which data extracted from single‐cell RNA‐seq (scRNA‐seq) gene expression data sets have been widely used to predict cellular tropism. The analysis presented here indicates that the SARS‐CoV‐2 cellular tropism predictions are accurate enough for estimating the potential susceptibility of different cells to SARS‐CoV‐2 infection; however, it appears that not all susceptible cells may be infected in patients with COVID‐19. [ABSTRACT FROM AUTHOR]

SARS-CoV-2 can infiltrate the lower respiratory tract, resulting in severe respiratory failure and a high death rate. Normally, the airway and alveolar epithelium can be rapidly reconstituted by multipotent stem cells after episodes of infection. Here, we analyzed published RNA-seq datasets and demonstrated that cells of four different lung epithelial stem cell types express SARS-CoV-2 entry factors, including Ace2. Thus, stem cells can be potentially infected by SARS-CoV-2, which may lead to defects in regeneration capacity partially accounting for the severity of SARS-CoV-2 infection and its consequences. [ABSTRACT FROM AUTHOR]