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The bidirectional association between the circadian system and innate-adaptive immune functions has been highlighted in many investigations. Viruses are a submicroscopic infectious agent that activate the immune system after entering the human host cell. A novel virus, so-called Coronavirus Disease 2019 (COVID-19), which has recently emerged, is an infectious disease caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Previous investigations show that the factors that are strongly controlled by circadian rhythms, such as clock genes and melatonin, modulate the immune response and may, therefore, influence the healing processes of COVID-19. Moreover, the mechanism of COVID-19 shows that some host cell factors, such as an angiotensin-converting enzyme, exhibit daily rhythms. In this review, we explore key findings that show a link between circadian rhythms and viral infection. The results of these findings could be helpful for clinical and preclinical studies to discover a useful and highly effective treatment for eradicating the COVID-19 disease.

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Introduction: In this systematic review, we will discuss the change of stroke incidence during the COVID-19 pandemic period and the proposed mechanisms of the relationship between SARS-CoV-2 and stroke.
Methods: Web of Science, PMC/Medline, and Scopus databases were searched until July 2020 without time and language limitations. After quality assessment, 22 articles were included in this study.
Results: Based on the results, it is impossible to conclude any definite relationship between the rising or decreasing stroke frequency or the shift in the ischemic and hemorrhagic ratio and SARS-CoV-2 infection. However, it appears that SARS-CoV-2 infection has some correlation with stroke. The supposed mechanisms for the SARS-CoV-2-related hemorrhagic stroke include 1) SARS-CoV-2-related vasculopathy with the endothelial damage of small vessels, 2) viral infection-induced platelet dysfunction or thrombocytopenia, and 3) activation of the proinflammatory cascade leading to coagulopathy. The helpful strategies are receiving therapeutic anticoagulation for high D-dimer or a known thrombus due to SARS-CoV-2 infection, as well as using extracorporeal membrane oxygenation (ECMO) in some patients. Furthermore, the possible mechanisms for the SARS-CoV-2-related ischemic stroke include 1) dysregulation of angiotensin-converting enzyme 2 (a key host cellular receptor for SARS-CoV-2)-related physiologic functions, 2) endothelial cell damages, 3) thrombo-inflammation, and 4) coagulopathy and coagulation abnormalities related to SARS-CoV-2 infection. 
Conclusion: A better understanding of the SARS-CoV-2 pathogenesis and its relation to neurologic abnormalities such as stroke can help to design new therapeutic approaches.