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It is too soon to attribute ADE to COVID-19

Identifieur interne : 000500 ( Pmc/Corpus ); précédent : 000499; suivant : 000501

It is too soon to attribute ADE to COVID-19

Auteurs : Anuj Sharma

Source :

RBID : PMC:7131212
Url:
DOI: 10.1016/j.micinf.2020.03.005
PubMed: 32268188
PubMed Central: 7131212

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PMC:7131212

Le document en format XML

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<name sortKey="Bottaccioli, F" uniqKey="Bottaccioli F">F. Bottaccioli</name>
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<name sortKey="Bianchi, M" uniqKey="Bianchi M">M. Bianchi</name>
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<name sortKey="Rovesti, M" uniqKey="Rovesti M">M. Rovesti</name>
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<name sortKey="Channappanavar, R" uniqKey="Channappanavar R">R. Channappanavar</name>
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<name sortKey="Mack, M" uniqKey="Mack M">M. Mack</name>
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<name sortKey="Zhao, J" uniqKey="Zhao J">J. Zhao</name>
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<journal-id journal-id-type="nlm-ta">Microbes Infect</journal-id>
<journal-id journal-id-type="iso-abbrev">Microbes Infect</journal-id>
<journal-title-group>
<journal-title>Microbes and Infection</journal-title>
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<issn pub-type="ppub">1286-4579</issn>
<issn pub-type="epub">1769-714X</issn>
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<publisher-name>Institut Pasteur. Published by Elsevier Masson SAS.</publisher-name>
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<article-id pub-id-type="pmid">32268188</article-id>
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<article-id pub-id-type="doi">10.1016/j.micinf.2020.03.005</article-id>
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<article-title>It is too soon to attribute ADE to COVID-19</article-title>
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<contrib contrib-type="author" id="au1">
<name>
<surname>Sharma</surname>
<given-names>Anuj</given-names>
</name>
<email>anuj.sharma.ctr@usuhs.edu</email>
</contrib>
</contrib-group>
<aff id="aff1">Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA</aff>
<pub-date pub-type="pmc-release">
<day>5</day>
<month>4</month>
<year>2020</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="epub">
<day>5</day>
<month>4</month>
<year>2020</year>
</pub-date>
<history>
<date date-type="received">
<day>24</day>
<month>3</month>
<year>2020</year>
</date>
<date date-type="accepted">
<day>31</day>
<month>3</month>
<year>2020</year>
</date>
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<permissions>
<copyright-statement>© 2020 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.</copyright-statement>
<copyright-year>2020</copyright-year>
<copyright-holder>Institut Pasteur</copyright-holder>
<license>
<license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p>
</license>
</permissions>
<kwd-group id="kwrds0010">
<title>Keywords</title>
<kwd>ADE</kwd>
<kwd>SARS-CoV-2</kwd>
</kwd-group>
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<body>
<p id="p0010">In the article “Is COVID-19 receiving ADE from other coronaviruses?” author has suggested the possibility of antibody dependent enhancement (ADE) of SARS-COV-2 disease (COVID-19) as a potential mechanism of the increase in severity of the disease [
<xref rid="bib1" ref-type="bibr">1</xref>
]. Although it’s an interesting hypothesis, we should be careful in attributing ADE to enhanced severity of the current disease. As viruses from same group share cross reactivity, it is not uncommon to have cross reactive antibody responses [
<xref rid="bib2" ref-type="bibr">2</xref>
]. Outside of the dengue virus serotypes family, which has demonstrated ADE in animal models, the ADE of the viruses using sub-neutralizing antibody levels has largely been restricted to
<italic>in-vitro</italic>
experiments. Cell culture experiments are considered pre-requisite to moving forward to animal experiments, however, not always result is translated to
<italic>in-vivo</italic>
setup. There is lack of collective innate/adaptive immune response
<italic>in-vitro</italic>
, which is presented
<italic>in-vivo</italic>
and the intricate interactions drive the disease pathology. Deliberate reduction in the neutralizing antibody levels in
<italic>in-vitro</italic>
assays and lack of innate immune response from other cells may result in an artificial ADE in cell-culture. As COVID-19 spread across the globe a common pattern of underlying morbid conditions such as diabetes and cardiovascular conditions is appearing. Such underlying conditions are known to present immune response dysfunction [
<xref rid="bib3" ref-type="bibr">3</xref>
,
<xref rid="bib4" ref-type="bibr">4</xref>
]. As reported by Channappanavar et al., immune dysregulation may contribute to lethal pneumonia induction by SARS-CoV [
<xref rid="bib5" ref-type="bibr">5</xref>
]. To date, vaccines are the most effective way of protecting against infectious diseases. Improper attribution of ADE in the absence of robust demonstration in animal models may hinder/scuttle the efforts to develop effective vaccines against SARS-CoV-2 and or other viruses of human health importance.</p>
<p id="p0015">Opinions expressed herewith are those of the author and are not necessarily representative of those of the USUHS, DoD, or the United States Army, Navy or Air Force.</p>
<sec id="sec1">
<title>Conflict of interest</title>
<p id="intref0010a">Author declares no conflict of interest.</p>
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