Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the aetiological agent of the pandemic coronavirus disease 2019 (COVID-19), is a newly found member of theCoronaviridaefamily, and is closely related to, albeit with important differences from, SARS-CoV [1]. It enters human cells through the binding of surface spike (S) glycoprotein with angiotensin-converting enzyme 2 (ACE2) [2–4]. The distal S1 subunit of the S protein is responsible for receptor binding, while the transmembrane S2 subunit mediates fusion between the viral envelope and the target cell membrane following proteolytic cleavage by specific cellular enzymes such as transmembrane serine protease 2 for S protein priming [5]. As it is likely that expression levels of ACE2 affect the efficiency of virus attachment and entry, as well as disease severity [6], and the interactions between viral S protein and ACE2 may directly cause lung injury [7], ACE2 may be a potential target of therapeutic and preventative interventions [8].
In summary, the unique potential links between SARS-CoV-2, circadian rhythms and sleep have been reviewed, and suggest the possibility that both of these homeostatic processes may significantly modify the susceptibility to infection as well as the overall clinical manifestation of the disease. Therefore, implementation of healthy sleep measures as a protective strategy against infection, and early detection of patients at risk of more severe disease (e.g.night-shift workers or patients with OSA), may enable improved implementation of supportive measures and lead to better outcomes.
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