The Improbability of the Rapid Development of a Vaccine for SARS-CoV-2 (Editorial)

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Author(s)
Morris, KV
Griffith University Author(s)
Year published
2020
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The coronavirus SARS-CoV-2 (Cov-2) has emerged on the world stage as a pandemic. It is a highly infectious agent that can spread rapidly and has a mortality rate of ∼2%–5%. Similar to its cousin, SARS-CoV-1 (Cov-1), CoV-2 employs the angiotensin converting enzyme 2 (ACE2) receptor and the serine protease TMPRSS2 to infect lung epithelial cells. CoV-2 also infects lung endothelial cells and macrophages and monocytes.1 Intriguingly, macrophages do not express appreciable levels of ACE2 or TMPRSS2,1 suggesting that this virus might use an entirely different receptor and a serine protease other than TMPRSS2 to infect these immune ...
View more >The coronavirus SARS-CoV-2 (Cov-2) has emerged on the world stage as a pandemic. It is a highly infectious agent that can spread rapidly and has a mortality rate of ∼2%–5%. Similar to its cousin, SARS-CoV-1 (Cov-1), CoV-2 employs the angiotensin converting enzyme 2 (ACE2) receptor and the serine protease TMPRSS2 to infect lung epithelial cells. CoV-2 also infects lung endothelial cells and macrophages and monocytes.1 Intriguingly, macrophages do not express appreciable levels of ACE2 or TMPRSS2,1 suggesting that this virus might use an entirely different receptor and a serine protease other than TMPRSS2 to infect these immune cells. An alternative, and possibly more likely explanation, based on a plethora of past studies with other coronaviruses, is that Cov-2 employs antibody-dependent enhancement (ADE) to infect immune cells.2
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View more >The coronavirus SARS-CoV-2 (Cov-2) has emerged on the world stage as a pandemic. It is a highly infectious agent that can spread rapidly and has a mortality rate of ∼2%–5%. Similar to its cousin, SARS-CoV-1 (Cov-1), CoV-2 employs the angiotensin converting enzyme 2 (ACE2) receptor and the serine protease TMPRSS2 to infect lung epithelial cells. CoV-2 also infects lung endothelial cells and macrophages and monocytes.1 Intriguingly, macrophages do not express appreciable levels of ACE2 or TMPRSS2,1 suggesting that this virus might use an entirely different receptor and a serine protease other than TMPRSS2 to infect these immune cells. An alternative, and possibly more likely explanation, based on a plethora of past studies with other coronaviruses, is that Cov-2 employs antibody-dependent enhancement (ADE) to infect immune cells.2
View less >
Journal Title
Molecular Therapy
Volume
28
Issue
7
Copyright Statement
© 2020, The American Society of Gene & Cell Therapy. Published by Elsevier Inc. All rights reserved. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International Licence, which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited.
Subject
Biological sciences
Biomedical and clinical sciences