tetano
Editor, Senior Moderator
Inflammation
. 2022 Mar 23.
doi: 10.1007/s10753-022-01656-7. Online ahead of print.
SARS-CoV-2 Infection: Host Response, Immunity, and Therapeutic Targets
Pooja Shivshankar[SUP] 1 2 [/SUP], Harry Karmouty-Quintana[SUP] 2 3 [/SUP], Tingting Mills[SUP] 2 [/SUP], Marie-Francoise Doursout[SUP] 1 [/SUP], Yanyu Wang[SUP] 1 [/SUP], Agnieszka K Czopik[SUP] 1 [/SUP], Scott E Evans[SUP] 4 [/SUP], Holger K Eltzschig[SUP] 1 [/SUP], Xiaoyi Yuan[SUP] 5 [/SUP]
Affiliations
Abstract
Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has resulted in a global pandemic with severe socioeconomic effects. Immunopathogenesis of COVID-19 leads to acute respiratory distress syndrome (ARDS) and organ failure. Binding of SARS-CoV-2 spike protein to human angiotensin-converting enzyme 2 (hACE2) on bronchiolar and alveolar epithelial cells triggers host inflammatory pathways that lead to pathophysiological changes. Proinflammatory cytokines and type I interferon (IFN) signaling in alveolar epithelial cells counter barrier disruption, modulate host innate immune response to induce chemotaxis, and initiate the resolution of inflammation. Here, we discuss experimental models to study SARS-CoV-2 infection, molecular pathways involved in SARS-CoV-2-induced inflammation, and viral hijacking of anti-inflammatory pathways, such as delayed type-I IFN response. Mechanisms of alveolar adaptation to hypoxia, adenosinergic signaling, and regulatory microRNAs are discussed as potential therapeutic targets for COVID-19.
Keywords: COVID-19; SARS-CoV-2; host responses; immunity.; inflammation.
. 2022 Mar 23.
doi: 10.1007/s10753-022-01656-7. Online ahead of print.
SARS-CoV-2 Infection: Host Response, Immunity, and Therapeutic Targets
Pooja Shivshankar[SUP] 1 2 [/SUP], Harry Karmouty-Quintana[SUP] 2 3 [/SUP], Tingting Mills[SUP] 2 [/SUP], Marie-Francoise Doursout[SUP] 1 [/SUP], Yanyu Wang[SUP] 1 [/SUP], Agnieszka K Czopik[SUP] 1 [/SUP], Scott E Evans[SUP] 4 [/SUP], Holger K Eltzschig[SUP] 1 [/SUP], Xiaoyi Yuan[SUP] 5 [/SUP]
Affiliations
- PMID: 35320469
- DOI: 10.1007/s10753-022-01656-7
Abstract
Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has resulted in a global pandemic with severe socioeconomic effects. Immunopathogenesis of COVID-19 leads to acute respiratory distress syndrome (ARDS) and organ failure. Binding of SARS-CoV-2 spike protein to human angiotensin-converting enzyme 2 (hACE2) on bronchiolar and alveolar epithelial cells triggers host inflammatory pathways that lead to pathophysiological changes. Proinflammatory cytokines and type I interferon (IFN) signaling in alveolar epithelial cells counter barrier disruption, modulate host innate immune response to induce chemotaxis, and initiate the resolution of inflammation. Here, we discuss experimental models to study SARS-CoV-2 infection, molecular pathways involved in SARS-CoV-2-induced inflammation, and viral hijacking of anti-inflammatory pathways, such as delayed type-I IFN response. Mechanisms of alveolar adaptation to hypoxia, adenosinergic signaling, and regulatory microRNAs are discussed as potential therapeutic targets for COVID-19.
Keywords: COVID-19; SARS-CoV-2; host responses; immunity.; inflammation.