Skip to main content
. 2021 Oct 29;15:770387. doi: 10.3389/fncel.2021.770387

FIGURE 1.

FIGURE 1

Several SARS-CoV-2 antigens interact directly with host EC proteins, inducing cellular senescence and altering the BBB permeability. Viral hijacking of furin/plasmin by antigen S2 impairs BDNF maturation, increasing PTSD susceptibility. The S1/ACE-2 attachment upregulates ANG II, inducing mitochondrial damage and cellular senescence. Viral ORF9b disrupts mitochondria directly, altering antiviral defenses and cellular metabolism. The SARS-CoV-2 antigen E exploits host epigenetic readers BRD-2 and BRD-4, altering the expression of mitochondrial proteins encoded in the nuclear DNA. Viral antigen NSP6 interacts with Sigma-1 receptors, inducing cellular senescence by an alternative pathway.