[18]
The neuro-targeting nature of the virus can explain the correlation of
SARS-COV-2 severity and the ischemic stroke due to the vascular injury
and the hyperimmune response. These responses alter the blood-brain
barrier permitting the virus to bind to the ACE2 receptor in the glial
cells, which, in addition to the hypercoagulation, plays an important
role in the development of ischemic stroke. [11,15].
Although the underlying pathophysiological process responsible for the
development of stroke in COVID-19 has not yet been determined, different
mechanisms related to the COVID-19 infectious process were postulated,
such as the host’s hyperinflammatory response with the exaggerated
cytokine release. For instance, interleukins play an essential role in
the inflammatory response, and COVID-19 patients; IL-1, a
macrophage-secreted interleukin, is elevated, especially in severe
COVID-19 cases. [4] Other inflammatory mediators
responsible for activating acute-phase reactions like interferon-gamma[5] , tumor necrosis factor-alpha, and IL-6 were also
elevated in SARS-COV-2 infected patients [8,9] . IL-6
activity has a unique importance as it’s considered a target for
tocilizumab, an IL-6 receptor antagonist with possible alleviation of
the SARS-COV2-associated cytokines storm and subsequently the severity
of the infection.[20].
Jenny et al. has addressed the relationship between the Inflammatory
cytokines and risk for ischemic stroke risk in their cohort study. They
found that raised IL-6 levels were associated with increased risk of
ischemic stroke (mean 4.5 vs. 3.7ng/mL; p < 0.001)[14]. Another factor supporting this association is the
endothelial injury, as described by Varga et al., where the
histopathology of different samples from three patients with SARS-COV2
infection confirmed evidence of viral endothelial invasion with
subsequent accumulation of the inflammatory cells attributed to the
widespread of ACE2 receptors through the endothelial vascular lining