Fig. 3.

Innate Immune Activation in SARS-CoV-2 Infection. The SARS-CoV-2 virus gains entry to cells by (1) binding to angiotensin converting enzyme 2 (ACE2) receptors on the cell surface through endocytosis or membrane fusion. (2) After entry the (+ sense) viral genome is released into the cytoplasm, (3) ribosomes (periwinkle) bind to viral genome to translate viral message into viral polymerase protein (light blue) and (4) RNA replication to produce (- sense) RNA genomes. A hyper inflammatory response can occur in SARS-CoV-2 infection and the presence of viral genomic and subgenomic RNA species activate cytosolic sensors such as toll-like receptor 3, 7 and 8 (TLR3/TLR7/TKR8). The activation of TRAF-6 leads to nuclear localization of NF-kB, IRF5 and IRF7 to induce expression of interferon stimulated genes that encode antiviral proteins and pro-inflammatory cytokines. Activation of TRAF-3 causes IRF3 to assume nuclear localization to stimulate production of Type I/II interferons. Produced using BioRender.com and adapted from a template provided by Natalya Odoardi Clinical Research Coordinator, Children’s Hospital of London