Fig. 1

Inflammatory phenomena associated with SARS-CoV-2 infection and its neurological and respiratory manifestations. The SARS-CoV-2 virus mainly enters the respiratory tract and reaches the lungs through direct ventilation and the CNS through the olfactory and trigeminal nerves. The entry of the virus is facilitated by NRP-1, ACE2 receptors, and protein S activation by TMPRSS2. In the CNS, the virus infects neurons, glial cells, and endothelial cells, increasing the permeability of the BBB. This may cause cerebral edema, intracranial hypertension, and neuroinflammation. If the viral infection continues, the damage spreads throughout the body, causing heart and systemic failure. This damage is associated with increased neuroinflammation directed by microglia and oligodendrocytes, causing damage to the brain stem and dysfunction of the heart and lungs. The exacerbated inflammation and intravascular coagulation induce respiratory arrest, possibly leading to the patient’s death. The inflammation is triggered by viral components (PAMPS) that activate TLR3, 7, and 8 receptors on the cell surface. Consequently, there is an increased production of pro-inflammatory cytokines (TNFα and IL 1β) and ROS, which can modify the P2X7 receptor in the brain and activate the inflammasome by the decrease of K^+. The activation of the inflammasome increases the production of IL-6 and pyroptosis. This diagram is based on the knowledge at the time of writing the manuscript