Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity
Identifieur interne : 000122 ( Main/Exploration ); précédent : 000121; suivant : 000123Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity
Auteurs : James Lyons-WeilerSource :
- Journal of Translational Autoimmunity [ 2589-9090 ] ; 2020.
Abstract
Homology between human and viral proteins is an established factor in viral- or vaccine-induced autoimmunity. Failure of SARS and MERS vaccines in animal trials involved pathogenesis consistent with an immunological priming that could involve autoimmunity in lung tissues due to previous exposure to the SARS and MERS spike protein. Exposure pathogenesis to SARS-CoV-2 in COVID-19 likely will lead to similar outcomes. Immunogenic peptides in viruses or bacteria that match human proteins are good candidates for pathogenic priming peptides (similar to the more diffuse idea of “immune enhancement”). Here I provide an assessment of potential for human pathogenesis via autoimmunity via exposure, via infection or injection. SAR-CoV-2 spike proteins, and all other SARS-CoV-2 proteins, immunogenic epitopes in each SARS-CoV-2 protein were compared to human proteins in search of high local homologous matching. Only one immunogenic epitope in a SARS-CoV-2 had no homology to human proteins. If all of the parts of the epitopes that are homologous to human proteins are excluded from consideration due to risk of pathogenic priming, the remaining immunogenic parts of the epitopes may be still immunogenic and remain as potentially viable candidates for vaccine development. Mapping of the genes encoding human protein matches to pathways point to targets that could explain the observed presentation of symptoms in COVID-19 disease. It also strongly points to a large number of opportunities for expected disturbances in the immune system itself, targeting elements of MHC Class I and Class II antigen presentation, PD-1 signaling, cross-presentation of soluble exogenous antigens and the ER-Phagosome pathway. Translational consequences of these findings are explored.
Url:
DOI: 10.1016/j.jtauto.2020.100051
PubMed: 32292901
PubMed Central: 7142689
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Pmc, to step Corpus: 000723
- to stream Pmc, to step Curation: 000723
- to stream Pmc, to step Checkpoint: 000049
- to stream PubMed, to step Corpus: 000024
- to stream PubMed, to step Curation: 000024
- to stream PubMed, to step Checkpoint: 000120
- to stream Ncbi, to step Merge: 002809
- to stream Ncbi, to step Curation: 002809
- to stream Ncbi, to step Checkpoint: 002809
- to stream Main, to step Merge: 000125
- to stream Main, to step Curation: 000122
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity</title>
<author><name sortKey="Lyons Weiler, James" sort="Lyons Weiler, James" uniqKey="Lyons Weiler J" first="James" last="Lyons-Weiler">James Lyons-Weiler</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">32292901</idno>
<idno type="pmc">7142689</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7142689</idno>
<idno type="RBID">PMC:7142689</idno>
<idno type="doi">10.1016/j.jtauto.2020.100051</idno>
<date when="2020">2020</date>
<idno type="wicri:Area/Pmc/Corpus">000723</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000723</idno>
<idno type="wicri:Area/Pmc/Curation">000723</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000723</idno>
<idno type="wicri:Area/Pmc/Checkpoint">000049</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000049</idno>
<idno type="wicri:source">PubMed</idno>
<idno type="RBID">pubmed:32292901</idno>
<idno type="wicri:Area/PubMed/Corpus">000024</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000024</idno>
<idno type="wicri:Area/PubMed/Curation">000024</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000024</idno>
<idno type="wicri:Area/PubMed/Checkpoint">000120</idno>
<idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000120</idno>
<idno type="wicri:Area/Ncbi/Merge">002809</idno>
<idno type="wicri:Area/Ncbi/Curation">002809</idno>
<idno type="wicri:Area/Ncbi/Checkpoint">002809</idno>
<idno type="wicri:Area/Main/Merge">000125</idno>
<idno type="wicri:Area/Main/Curation">000122</idno>
<idno type="wicri:Area/Main/Exploration">000122</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity</title>
<author><name sortKey="Lyons Weiler, James" sort="Lyons Weiler, James" uniqKey="Lyons Weiler J" first="James" last="Lyons-Weiler">James Lyons-Weiler</name>
</author>
</analytic>
<series><title level="j">Journal of Translational Autoimmunity</title>
<idno type="eISSN">2589-9090</idno>
<imprint><date when="2020">2020</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Homology between human and viral proteins is an established factor in viral- or vaccine-induced autoimmunity. Failure of SARS and MERS vaccines in animal trials involved pathogenesis consistent with an immunological priming that could involve autoimmunity in lung tissues due to previous exposure to the SARS and MERS spike protein. Exposure pathogenesis to SARS-CoV-2 in COVID-19 likely will lead to similar outcomes. Immunogenic peptides in viruses or bacteria that match human proteins are good candidates for pathogenic priming peptides (similar to the more diffuse idea of “immune enhancement”). Here I provide an assessment of potential for human pathogenesis via autoimmunity via exposure, via infection or injection. SAR-CoV-2 spike proteins, and all other SARS-CoV-2 proteins, immunogenic epitopes in each SARS-CoV-2 protein were compared to human proteins in search of high local homologous matching. Only one immunogenic epitope in a SARS-CoV-2 had no homology to human proteins. If all of the parts of the epitopes that are homologous to human proteins are excluded from consideration due to risk of pathogenic priming, the remaining immunogenic parts of the epitopes may be still immunogenic and remain as potentially viable candidates for vaccine development. Mapping of the genes encoding human protein matches to pathways point to targets that could explain the observed presentation of symptoms in COVID-19 disease. It also strongly points to a large number of opportunities for expected disturbances in the immune system itself, targeting elements of MHC Class I and Class II antigen presentation, PD-1 signaling, cross-presentation of soluble exogenous antigens and the ER-Phagosome pathway. Translational consequences of these findings are explored.</p>
</div>
</front>
<back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Shi, H" uniqKey="Shi H">H. Shi</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Deming, D" uniqKey="Deming D">D. Deming</name>
</author>
<author><name sortKey="Sheahan, T" uniqKey="Sheahan T">T. Sheahan</name>
</author>
<author><name sortKey="Heise, M" uniqKey="Heise M">M. Heise</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Weingartl, H" uniqKey="Weingartl H">H. Weingartl</name>
</author>
<author><name sortKey="Czub, M" uniqKey="Czub M">M. Czub</name>
</author>
<author><name sortKey="Czub, S" uniqKey="Czub S">S. Czub</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Yao, B" uniqKey="Yao B">B. Yao</name>
</author>
<author><name sortKey="Zhang, L" uniqKey="Zhang L">L. Zhang</name>
</author>
<author><name sortKey="Liang, S" uniqKey="Liang S">S. Liang</name>
</author>
<author><name sortKey="Svmtrip, C Zhang" uniqKey="Svmtrip C">C. Zhang SVMTriP</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Ahmed, S S" uniqKey="Ahmed S">S.S. Ahmed</name>
</author>
<author><name sortKey="Volkmuth, W" uniqKey="Volkmuth W">W. Volkmuth</name>
</author>
<author><name sortKey="Duca, J" uniqKey="Duca J">J. Duca</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Agrawal, A S" uniqKey="Agrawal A">A.S. Agrawal</name>
</author>
<author><name sortKey="Tao, X" uniqKey="Tao X">X. Tao</name>
</author>
<author><name sortKey="Algaissi, A" uniqKey="Algaissi A">A. Algaissi</name>
</author>
</analytic>
</biblStruct>
</listBibl>
</div1>
</back>
</TEI>
<affiliations><list></list>
<tree><noCountry><name sortKey="Lyons Weiler, James" sort="Lyons Weiler, James" uniqKey="Lyons Weiler J" first="James" last="Lyons-Weiler">James Lyons-Weiler</name>
</noCountry>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/MersV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000122 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000122 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Sante |area= MersV1 |flux= Main |étape= Exploration |type= RBID |clé= PMC:7142689 |texte= Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:32292901" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \ | NlmPubMed2Wicri -a MersV1
This area was generated with Dilib version V0.6.33. |