A Comprehensive Review of Viral Characteristics, Transmission, Pathophysiology, Immune Response, and Management of SARS-CoV-2 and COVID-19 as a Basis for Controlling the Pandemic
Open Access
- 26 February 2021
- journal article
- review article
- Published by Frontiers Media SA in Frontiers in Immunology
- Vol. 12, 631139
- https://doi.org/10.3389/fimmu.2021.631139
Abstract
COVID-19 emerged from China in December 2019 and during 2020 spread to every continent including Antarctica. The coronavirus, SARS-CoV-2, has been identified as the causative pathogen, and its spread has stretched the capacities of healthcare systems and negatively affected the global economy. This review provides an update on the virus, including the genome, the risks associated with the emergence of variants, mode of transmission, immune response, COVID-19 in children and the elderly, and advances made to contain, prevent and manage the disease. Although our knowledge of the mechanics of virus transmission and the immune response has been substantially demystified, concerns over reinfection, susceptibility of the elderly and whether asymptomatic children promote transmission remain unanswered. There are also uncertainties about the pathophysiology of COVID-19 and why there are variations in clinical presentations and why some patients suffer from long lasting symptoms—“the long haulers.” To date, there are no significantly effective curative drugs for COVID-19, especially after failure of hydroxychloroquine trials to produce positive results. The RNA polymerase inhibitor, remdesivir, facilitates recovery of severely infected cases but, unlike the anti-inflammatory drug, dexamethasone, does not reduce mortality. However, vaccine development witnessed substantial progress with several being approved in countries around the globe.This publication has 230 references indexed in Scilit:
- Lack of Innate Interferon Responses during SARS Coronavirus Infection in a Vaccination and Reinfection Ferret ModelPLOS ONE, 2012
- Evidence that TMPRSS2 Activates the Severe Acute Respiratory Syndrome Coronavirus Spike Protein for Membrane Fusion and Reduces Viral Control by the Humoral Immune ResponseJournal of Virology, 2011
- The SARS Coronavirus 3a Protein Causes Endoplasmic Reticulum Stress and Induces Ligand-Independent Downregulation of the Type 1 Interferon ReceptorPLOS ONE, 2009
- Characterization of a Highly Conserved Domain within the Severe Acute Respiratory Syndrome Coronavirus Spike Protein S2 Domain with Characteristics of a Viral Fusion PeptideJournal of Virology, 2009
- Severe Acute Respiratory Syndrome Coronavirus M Protein Inhibits Type I Interferon Production by Impeding the Formation of TRAF3·TANK·TBK1/IKKϵ ComplexOnline Journal of Public Health Informatics, 2009
- Cryo-electron tomography of mouse hepatitis virus: Insights into the structure of the coronavirionProceedings of the National Academy of Sciences of the United States of America, 2009
- SARS coronavirus and innate immunityVirus Research, 2008
- Severe Acute Respiratory Syndrome Coronavirus Evades Antiviral Signaling: Role of nsp1 and Rational Design of an Attenuated StrainJournal of Virology, 2007
- Supramolecular Architecture of Severe Acute Respiratory Syndrome Coronavirus Revealed by Electron CryomicroscopyJournal of Virology, 2006
- The time course of the immune response to experimental coronavirus infection of manEpidemiology and Infection, 1990