A review of the mechanisms of blood–brain barrier disruption during COVID‐19 infection

Abstract

Coronaviruses are prevalent in mammals and birds, including humans and bats, and they often spread through airborne droplets. In humans, these droplets then interact with angiotensin‐converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2), which are the main receptors for the SARS‐CoV‐2 virus. It can infect several organs, including the brain. The blood–brain barrier (BBB) is designed to maintain the homeostatic neural microenvironment of the brain, which is necessary for healthy neuronal activity, function, and stability. It prevents viruses from entering the brain parenchyma and does not easily allow chemicals to pass into the brain while assisting numerous compounds in exiting the brain. The purpose of this review was to examine how COVID‐19 influences the BBB along with the mechanisms that indicate the BBB's deterioration. In addition, the cellular mechanism through which SARS‐CoV‐2 causes BBB destruction by binding to ACE2 was evaluated and addressed. The mechanisms of the immunological reaction that occurs during COVID‐19 infection that may contribute to the breakdown of the BBB were also reviewed. It was discovered that the integrity of the tight junction (TJs), basement membrane, and adhesion molecules was damaged during COVID‐19 infection, which led to the breakdown of the BBB. Therefore, understanding how the BBB is disrupted by COVID‐19 infection will provide an indication of how the SARS‐CoV‐2 virus is able to reach the central nervous system (CNS). The findings of this research may help in the identification of treatment options for COVID‐19 that can control and manage the infection.

Intracranial granulomatous inflammation caused by cryptococcal infection: a case study and literature analysis

“…However, the patient experienced COVID-19 three months prior to disease onset, with monocyte/macrophage, dendritic-cell, mast-cell, and T-cell activation during infection, potentially triggering a hyperinflammatory cytokine storm response. Specifically, the severe acute respiratory syndrome-related coronavirus (SARS-CoV-2) spike protein caused blood-brain barrier instability in the brain endothelium, promoting a proinflammatory state ( 10 ). Although her symptoms of headache, hearing loss, and memory impairment were consistent with the common clinical manifestations of cryptococcal intracranial infection, the absence of fever and meningeal irritation symptoms hindered CSF testing, leading to diagnostic delays.…”