TY - JOUR T1 - SARS-CoV-2 infection activates the cyclic guanosine of monophosphate-adenosine monophosphate synthase-stimulator interferon genes pathway in the lung : a review AU - Aragão, Gislei F. AU - Feitosa, Sthefane G. AU - Veras, Herlice Do Nascimento AU - de Lima Filho, Cícero Gilmário A. P. AU - Assunção, Karinne da S. AU - Arrais, Luana M. AU - Teixeira, Sara Lívia M. Y1 - 2023/// JO - Exploration of Immunology VL - 3 IS - 1 SP - 56 EP - 69 DO - 10.37349/ei.2023.00089 UR - https://www.explorationpub.com/Journals/ei/Article/100389 AB - The infection of COVID-19 is directly linked to the destruction of lung epithelial cells, and the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes (cGAS-STING) system has been implicated in the pathology of respiratory infections. This study aimed to systematize the relationship between the pathophysiology of COVID-19 and the cGAS-STING system’s activation in the lungs. Severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is an RNA virus that belongs to the Coronaviridae family whose genetic material is produced by a single positive RNA molecule (RNA+). The cGAS-STING signaling pathway has emerged as a key mediator of injury caused by infection and cellular or tissue stress. The cGAS-STING cyclic pathway is part of innate immunity and is activated from cytosolic DNA responses present in newly formed syncytia, by cell-to-cell fusion, in target of angiotensin-converting enzyme 2 (ACE2) expression and SARS-CoV-2 Spike protein. Although this pathway is canonically understood to be responsive to both pathogen-derived and host-derived DNA, it has been demonstrated to cross-communicate with the retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs). cGAS-STING activation is significant to interferon production, mainly type-I interferons (IFN-I), in a SARS-CoV-2 infection scenario, indicating a major antiviral role of the cGAS-STING pathway. It was identified that in SARS-CoV-2 the cGAS-STING axis is activated, but the inflammatory response could be specific for nuclear factor-κB (NF-κB) in infected cells, and that this axis is potentiated by a cytokine storm produced by the immune system’s cells. ER -