The COVID-19 is a global pandemic. Its rapid dissemination and serious course require a novel approach to healthcare practices. Severe disease progression is often associated with the development of the Acute Respiratory Distress Syndrome and may require some form of respiratory support, including endotracheal intubation, mechanical ventilation, and enteral nutrition through a nasogastric tube. These conditions increase the risk of dysphagia, aspiration, and aspiration pneumonia. The data on the incidence and risks of dysphagia associated with COVID-19 are not yet available. However, it is assumed that these patients are at high risk, because of respiratory symptoms and reduced lung function. These findings may exacerbate swallowing deficits. The aim of this review is to summarize available information on possible mechanisms of postintubation dysphagia in COVID-19 patients. Recommendations regarding the diagnosis and management of postintubation dysphagia in COVID-19 patients are described in this contemporary review.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cell entry starts with membrane attachment and ends with spike (S) protein–catalyzed membrane fusion depending on two cleavage steps, namely, one usually by furin in producing cells and the second by TMPRSS2 on target cells. Endosomal cathepsins can carry out both. Using real-time three-dimensional single-virion tracking, we show that fusion and genome penetration require virion exposure to an acidic milieu of pH 6.2 to 6.8, even when furin and TMPRSS2 cleavages have occurred. We detect the sequential steps of S1-fragment dissociation, fusion, and content release from the cell surface in TMPRRS2-overexpressing cells only when exposed to acidic pH. We define a key role of an acidic environment for successful infection, found in endosomal compartments and at the surface of TMPRSS2-expressing cells in the acidic milieu of the nasal cavity.