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Severe acute respiratory syndrome coronavirus entry as a target of antiviral therapies Kuhn JH; Li W; Radoshitzky SR; Choe H; Farzan MAntivir Ther 2007[]; 12 (4 Pt B): 639-50The identification in 2003 of a coronavirus as the aetiological agent of severe acute respiratory syndrome (SARS) intensified efforts to understand the biology of coronaviruses in general and SARS coronavirus (SARS-CoV) in particular. Rapid progress was made in describing the SARS-CoV genome, evolution and lifecycle. Identification of angiotensin-converting enzyme 2 (ACE2) as an obligate cellular receptor for SARS-CoV contributed to understanding of the SARS-CoV entry process, and helped to characterize two targets of antiviral therapeutics: the SARS-CoV spike protein and ACE2. Here we describe the role of these proteins in SARS-CoV replication and potential therapeutic strategies aimed at preventing entry of SARS-CoV into target cells.|Angiotensin-Converting Enzyme 2[MESH]|Animals[MESH]|Antiviral Agents/*pharmacology/therapeutic use[MESH]|Cats[MESH]|Cattle[MESH]|Dogs[MESH]|Humans[MESH]|Membrane Glycoproteins/chemistry/*drug effects/metabolism[MESH]|Models, Molecular[MESH]|Peptidyl-Dipeptidase A/*drug effects/metabolism[MESH]|Rabbits[MESH]|Rats[MESH]|Receptors, Virus/*drug effects/metabolism[MESH]|Severe Acute Respiratory Syndrome/drug therapy/virology[MESH]|Severe acute respiratory syndrome-related coronavirus/drug effects/*pathogenicity[MESH]|Spike Glycoprotein, Coronavirus[MESH]|Viral Envelope Proteins/chemistry/*drug effects/metabolism[MESH] |
