Molecular mimicry between SARS-CoV-2 and respiratory pacemaker neurons

Lucchese, Guglielmo; Flöel, Agnes

doi:10.1016/j.autrev.2020.102556

Cited by 93 publications

(91 citation statements)

References 15 publications

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“…The former occurs when similarities between foreign and selfpeptides favor an activation of autoreactive T or B cells by foreignderived peptides in a susceptible individual [10]. The SARS-CoV-2 proteome was described as sharing three sequences of six amino acids (GSQASS, LNEVAK, and SAAEAS) with three proteins, namely DAB1, AIFM, and SURF1 which are present in the brainstem respiratory pacemaker, also known as the pre-Bötzinger complex [175]. The authors suggested that these partial but not complete similarities might account for an autoimmune mediated respiratory central depression.…”

Section: Autoimmunity In Covid-19mentioning

confidence: 99%

Autoinflammatory and autoimmune conditions at the crossroad of COVID-19

Rodríguez

Novelli

Rojas

et al. 2020

Journal of Autoimmunity

270

281

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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.

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Section: Autoimmunity In Covid-19mentioning

confidence: 99%

Autoinflammatory and autoimmune conditions at the crossroad of COVID-19

Rodríguez

Novelli

Rojas

et al. 2020

Journal of Autoimmunity

270

281

View full text Add to dashboard Cite

show abstract

“…Animal models revealed the route of neuropropagation from nasal cavity to olfactory bulb, piriform cortex and brainstem (Dube et al 2018;Netland et al 2008). Neurodestructive processes, including immune-mediated damage or exacerbated autoimmunity (Cao 2020;Toscano et al 2020;Troyer et al 2020;Lucchese and Floel 2020;Moldofsky and Patcai 2011;Lo et al 2006;Zhang et al 2020) may thereby well be initiated and contribute to neurodegenerative diseases like Morbus Alzheimer and other dementias as late consequences. Therefore, neuroprotective strategies should be initiated in severely affected COVID-19 patients without any delay.…”

Section: Epo: the Case For Neuroprotection In Covid-19mentioning

confidence: 99%

“…Brain invasion of SARS-CoV-2 may partially be responsible for the acute breathing failure of patients with COVID-19, with respiratory brainstem centers playing a prominent role. Associated neuropathy and myositis likely encompass phrenic nerve and respiratory muscles (Li et al 2020b;Mao et al 2020;Nath 2020;Lucchese and Floel 2020;.…”

Section: Introductionmentioning

confidence: 99%

Erythropoietin as candidate for supportive treatment of severe COVID-19

Ehrenreich

Weißenborn

Begemann

et al. 2020

Mol Med

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In light of the present therapeutic situation in COVID-19, any measure to improve course and outcome of seriously affected individuals is of utmost importance. We recap here evidence that supports the use of human recombinant erythropoietin (EPO) for ameliorating course and outcome of seriously ill COVID-19 patients. This brief expert review grounds on available subject-relevant literature searched until May 14, 2020, including Medline, Google Scholar, and preprint servers. We delineate in brief sections, each introduced by a summary of respective COVID-19 references, how EPO may target a number of the gravest sequelae of these patients. EPO is expected to: (1) improve respiration at several levels including lung, brainstem, spinal cord and respiratory muscles; (2) counteract overshooting inflammation caused by cytokine storm/ inflammasome; (3) act neuroprotective and neuroregenerative in brain and peripheral nervous system. Based on this accumulating experimental and clinical evidence, we finally provide the research design for a double-blind placebo-controlled randomized clinical trial including severely affected patients, which is planned to start shortly.

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“…To the Editor, Molecular mimicry has been proposed as a cause of the autoimmune phenomena observed in COVID-19 [1][2][3][4], the syndrome associated with the infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Lucchese and Flöel [4] have recently reported three human proteins (namely DAB1, AIFM, and SURF1, as catalogued at www.uniprot.org) -that are present in neurons of the respiratory pacemaker in the brainstem -that share potentially antigenic epitopes with SARS-CoV-2, as shown by in silico analysis.…”

mentioning

confidence: 99%