Understanding the Role of Blood Vessels in the Neurologic Manifestations of Coronavirus Disease 2019 (COVID-19)

Abstract

SARS-CoV-2 was originally identified as an outbreak in Wuhan, China towards the end of 2019 and quickly became a global pandemic, with a large death toll. Originally identified as a respiratory disease, similar to previously discovered SARS and MERS type viruses, concern has since been raised about the effects of SARS-CoV-2 infection on the vasculature. This viral-vascular involvement is of particular concern with regards to the small vessels present in the brain, with mounting evidence demonstrating that SARS-CoV-2 is capable of crossing the blood-brain-barrier. Severe symptoms of infection, termed COVID-19, often result in neurological complications, regardless of patient age. These neurological complications range from mild to severe across all demographics, however, the long-term repercussions of neurological involvement on patient health are still unknown.

Safe and Effective Disease-Modifying Therapies for Small Blood Vessel Disease in the Brain

“…Finally, the contribution of Kim and Whitmore reviews the rapidly evolving field of vascular consequences of infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). 11 As noted in this article, the next few years will tell us more about intriguing neurovascular effects of SARS-CoV-2 and how they impact cognition.…”

COVID-19 infection in patients with chronic obstructive pulmonary disease: From pathophysiology to therapy. Mini-review

“…COPD patients who are former smokers tend to exhibit the highest mortality associated with COVID-19 infection [15][16][17]. The pathophysiological mechanisms by which smoking increases the risk of developing complications from COVID-19 include impaired innate and adaptive immune responses and impairment of the lungs' self-cleansing defense mechanisms [25,26] (Table 1). Inhaled steroids in COPD do not increase susceptibility to viral infection and that in any case; the prescribed basal therapy should not be abandoned during a coronavirus pandemic.…”

“…It is important to highlight the pathogenic role of endothelitis associated with diffuse infection and inflammation of the endothelium, which can lead to activation of the coagulation system and the complement cascade, resulting in vascular injury and thromboembolism, ischemia, thus increasing further organ damage in patients [22,23]. A recently recognized important feature of COVID-19 is the abnormal activation of the coagulation system, which clinically predisposes to arterial and venous thromboembolism [24][25][26][27][28]. The degree of coagulopathy is proportional to the severity of the disease and thromboinflammatory biomarkers predict worse outcomes [29].…”

Neuroinflammation and COVID-19 Ischemic Stroke Recovery—Evolving Evidence for the Mediating Roles of the ACE2/Angiotensin-(1–7)/Mas Receptor Axis and NLRP3 Inflammasome

“…A recent report from genomic studies suggested that the genetic sources of α- and β-coronaviruses (CoVs) were derived from bats and rodents, and from an avian host in the case of δ- and γ-CoVs [ 11 ]. Moreover, about seven human CoVs have been recognized that potentially cause mild-to-severe diseases (including neurological disease) in various animal species such as cats, camels, and cows (including cattle) [ 12 ]. Alarmingly, recent scientific evidence has shown that these CoVs are accountable for nearly 10% of acute respiratory infections [ 11 , 13 ], and about 15% of individuals infected by members of the genus β-CoVs (i.e., SARS-CoV-2 and Middle East respiratory syndrome coronavirus (MERS-CoVs)) will develop severe disease, among whom 6% become critically ill [ 11 , 14 ].…”