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Plasmapheresis, Anti-ACE2 and Anti-FcγRII Monoclonal Antibodies: A Possible Treatment for Severe Cases of COVID-19

Authors Sedokani A, Feizollahzadeh S

Received 12 May 2020

Accepted for publication 26 June 2020

Published 6 July 2020 Volume 2020:14 Pages 2607—2611


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Jianbo Sun

Amin Sedokani,1 Sadegh Feizollahzadeh2

1Cardiology Department, Medical Faculty, Urmia University of Medical Sciences, Urmia, Iran; 2Medical Immunology, Laboratory Sciences, School of Allied Medical Sciences, Urmia University of Medical Sciences, Urmia, Iran

Correspondence: Amin Sedokani
Cardiology Department, Medical Faculty, Urmia University of Medical Sciences, 17 Sharivar St., Urmia 571478334, Iran
Tel +98 443237 5907
Fax +98 443 237 2917
Email [email protected]

Abstract: In March 2020, the WHO declared the COVID-19 disease as a pandemic disease. There have been studies on the COVID-19 to find a certain treatment, but yet, there is no certain cure. In this article, we present a possible way to treat severe cases of COVID-19. Based on the previous studies, there are similarities between the spike antigens of SARS-CoV and SARS-CoV-2 viruses. It is expected that these similarities (structural and affinity to the receptor of ACE2) can lead to the same pathophysiological activity of the virus by the use of ACE2 and FcγRII (the antibody-dependent enhancement mechanism). Therefore, we propose a way of washing out (by plasmapheresis) the possible antibodies against the spike protein of the virus out of patients’ plasma to stop the antibody-dependent enhancement (ADE)-mediated infection of the immune system cells at the first phase of the treatment and simultaneous use of the anti-ACE2 with anti-FcγRII monoclonal antibodies at the second phase. We propose these procedures for the patients that have no significant response for typical anti-viral, ARDS and conservative therapies, and the disease persists or progresses despite sufficient therapies.

Keywords: COVID-19, SARS-CoV-2, antibody-dependent enhancement, plasmapheresis, monoclonal antibodies

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