¿Es esperable que haya cuadros neurológicos por la pandemia por SARS-CoV-2?
Identifieur interne : 001265 ( Pmc/Corpus ); précédent : 001264; suivant : 001266¿Es esperable que haya cuadros neurológicos por la pandemia por SARS-CoV-2?
Auteurs : J. Matías-Guiu ; U. Gomez-Pinedo ; P. Montero-Escribano ; P. Gomez-Iglesias ; J. Porta-Etessam ; J. A. Matias-GuiuSource :
- Neurologia (Barcelona, Spain) [ 0213-4853 ] ; 2020.
Abstract
Diversas evidencias sugieren que el SARS-CoV-2 puede penetrar en el sistema nervioso central (SNC). Los autores revisan los datos de la literatura sobre los hallazgos de coronavirus en el SNC asociado a enfermedades neurológicas.
En las distintas epidemias con SARS-CoV y MERS-CoV la presencia de cuadros neurológicos es baja, pero se describen cuadros aislados de pacientes. También existen casos asociados a OC43-CoV y 229E-CoV. La existencia de lesiones neurológicas, especialmente desmielinizantes en el modelo MHV-CoV pueden explicar mecanismos de penetración de los CoV en el SNC y especialmente aquellos relacionados con la respuesta inmune, que puede justificar la existencia de CoV en pacientes con esclerosis múltiple. Los autores revisan aspectos diferenciales de SARS-CoV-2 y se plantean si debido al alto número de infectados, el virus puede afectar de forma mayor al SNC.
Aunque la presencia de síntomas neurológicos en las epidemias de CoV es baja, la mayor frecuencia de infectados por SARS-CoV-2 podría justificar el paso del virus y la posibilidad de clínica neurológica precoz o tardía con mayor incidencia. El seguimiento de los pacientes de la epidemia debe atender con cuidado a la evaluación del SNC.
Url:
DOI: 10.1016/j.nrl.2020.03.001
PubMed: 32299636
PubMed Central: 7136883
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">¿Es esperable que haya cuadros neurológicos por la pandemia por SARS-CoV-2?</title><author><name sortKey="Matias Guiu, J" sort="Matias Guiu, J" uniqKey="Matias Guiu J" first="J." last="Matías-Guiu">J. Matías-Guiu</name></author><author><name sortKey="Gomez Pinedo, U" sort="Gomez Pinedo, U" uniqKey="Gomez Pinedo U" first="U." last="Gomez-Pinedo">U. Gomez-Pinedo</name></author><author><name sortKey="Montero Escribano, P" sort="Montero Escribano, P" uniqKey="Montero Escribano P" first="P." last="Montero-Escribano">P. Montero-Escribano</name></author><author><name sortKey="Gomez Iglesias, P" sort="Gomez Iglesias, P" uniqKey="Gomez Iglesias P" first="P." last="Gomez-Iglesias">P. Gomez-Iglesias</name></author><author><name sortKey="Porta Etessam, J" sort="Porta Etessam, J" uniqKey="Porta Etessam J" first="J." last="Porta-Etessam">J. Porta-Etessam</name></author><author><name sortKey="Matias Guiu, J A" sort="Matias Guiu, J A" uniqKey="Matias Guiu J" first="J. A." last="Matias-Guiu">J. A. Matias-Guiu</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">32299636</idno><idno type="pmc">7136883</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7136883</idno><idno type="RBID">PMC:7136883</idno><idno type="doi">10.1016/j.nrl.2020.03.001</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">001265</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001265</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">¿Es esperable que haya cuadros neurológicos por la pandemia por SARS-CoV-2?</title><author><name sortKey="Matias Guiu, J" sort="Matias Guiu, J" uniqKey="Matias Guiu J" first="J." last="Matías-Guiu">J. Matías-Guiu</name></author><author><name sortKey="Gomez Pinedo, U" sort="Gomez Pinedo, U" uniqKey="Gomez Pinedo U" first="U." last="Gomez-Pinedo">U. Gomez-Pinedo</name></author><author><name sortKey="Montero Escribano, P" sort="Montero Escribano, P" uniqKey="Montero Escribano P" first="P." last="Montero-Escribano">P. Montero-Escribano</name></author><author><name sortKey="Gomez Iglesias, P" sort="Gomez Iglesias, P" uniqKey="Gomez Iglesias P" first="P." last="Gomez-Iglesias">P. Gomez-Iglesias</name></author><author><name sortKey="Porta Etessam, J" sort="Porta Etessam, J" uniqKey="Porta Etessam J" first="J." last="Porta-Etessam">J. Porta-Etessam</name></author><author><name sortKey="Matias Guiu, J A" sort="Matias Guiu, J A" uniqKey="Matias Guiu J" first="J. A." last="Matias-Guiu">J. A. Matias-Guiu</name></author></analytic><series><title level="j">Neurologia (Barcelona, Spain)</title><idno type="ISSN">0213-4853</idno><idno type="eISSN">1578-1968</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Resumen</title><sec><title>Introducción</title><p>Diversas evidencias sugieren que el SARS-CoV-2 puede penetrar en el sistema nervioso central (SNC). Los autores revisan los datos de la literatura sobre los hallazgos de coronavirus en el SNC asociado a enfermedades neurológicas.</p></sec><sec><title>Desarrollo</title><p>En las distintas epidemias con SARS-CoV y MERS-CoV la presencia de cuadros neurológicos es baja, pero se describen cuadros aislados de pacientes. También existen casos asociados a OC43-CoV y 229E-CoV. La existencia de lesiones neurológicas, especialmente desmielinizantes en el modelo MHV-CoV pueden explicar mecanismos de penetración de los CoV en el SNC y especialmente aquellos relacionados con la respuesta inmune, que puede justificar la existencia de CoV en pacientes con esclerosis múltiple. Los autores revisan aspectos diferenciales de SARS-CoV-2 y se plantean si debido al alto número de infectados, el virus puede afectar de forma mayor al SNC.</p></sec><sec><title>Conclusión</title><p>Aunque la presencia de síntomas neurológicos en las epidemias de CoV es baja, la mayor frecuencia de infectados por SARS-CoV-2 podría justificar el paso del virus y la posibilidad de clínica neurológica precoz o tardía con mayor incidencia. El seguimiento de los pacientes de la epidemia debe atender con cuidado a la evaluación del SNC.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Corman, V M" uniqKey="Corman V">V.M. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Neurologia</journal-id><journal-id journal-id-type="iso-abbrev">Neurologia</journal-id><journal-title-group><journal-title>Neurologia (Barcelona, Spain)</journal-title></journal-title-group><issn pub-type="ppub">0213-4853</issn><issn pub-type="epub">1578-1968</issn><publisher><publisher-name>Published by Elsevier España, S.L.U. on behalf of Sociedad Española de Neurología.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32299636</article-id><article-id pub-id-type="pmc">7136883</article-id><article-id pub-id-type="publisher-id">S0213-4853(20)30065-7</article-id><article-id pub-id-type="doi">10.1016/j.nrl.2020.03.001</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>¿Es esperable que haya cuadros neurológicos por la pandemia por SARS-CoV-2?</article-title><trans-title-group xml:lang="en"><trans-title>Should we expect neurological symptoms in the SARS-CoV-2 epidemic?</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" id="aut0005"><name><surname>Matías-Guiu</surname><given-names>J.</given-names></name><email>neurol.hcsc@salud.madrid.org</email><xref rid="cor0005" ref-type="corresp">⁎</xref></contrib><contrib contrib-type="author" id="aut0010"><name><surname>Gomez-Pinedo</surname><given-names>U.</given-names></name></contrib><contrib contrib-type="author" id="aut0015"><name><surname>Montero-Escribano</surname><given-names>P.</given-names></name></contrib><contrib contrib-type="author" id="aut0020"><name><surname>Gomez-Iglesias</surname><given-names>P.</given-names></name></contrib><contrib contrib-type="author" id="aut0025"><name><surname>Porta-Etessam</surname><given-names>J.</given-names></name></contrib><contrib contrib-type="author" id="aut0030"><name><surname>Matias-Guiu</surname><given-names>J.A.</given-names></name></contrib></contrib-group><aff id="aff0005">Servicio de Neurología, Instituto de Neurociencias, Hospital Clínico San Carlos, San Carlos, IdISSC, Madrid, España</aff><author-notes><corresp id="cor0005"><label>⁎</label>Autor para correspondencia. <email>neurol.hcsc@salud.madrid.org</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>6</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>6</day><month>4</month><year>2020</year></pub-date><history><date date-type="received"><day>27</day><month>3</month><year>2020</year></date><date date-type="accepted"><day>31</day><month>3</month><year>2020</year></date></history><permissions><copyright-statement>© 2020 Published by Elsevier España, S.L.U. on behalf of Sociedad Española de Neurología.</copyright-statement><copyright-year>2020</copyright-year><copyright-holder></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><abstract id="abs0010"><title>Resumen</title><sec><title>Introducción</title><p>Diversas evidencias sugieren que el SARS-CoV-2 puede penetrar en el sistema nervioso central (SNC). Los autores revisan los datos de la literatura sobre los hallazgos de coronavirus en el SNC asociado a enfermedades neurológicas.</p></sec><sec><title>Desarrollo</title><p>En las distintas epidemias con SARS-CoV y MERS-CoV la presencia de cuadros neurológicos es baja, pero se describen cuadros aislados de pacientes. También existen casos asociados a OC43-CoV y 229E-CoV. La existencia de lesiones neurológicas, especialmente desmielinizantes en el modelo MHV-CoV pueden explicar mecanismos de penetración de los CoV en el SNC y especialmente aquellos relacionados con la respuesta inmune, que puede justificar la existencia de CoV en pacientes con esclerosis múltiple. Los autores revisan aspectos diferenciales de SARS-CoV-2 y se plantean si debido al alto número de infectados, el virus puede afectar de forma mayor al SNC.</p></sec><sec><title>Conclusión</title><p>Aunque la presencia de síntomas neurológicos en las epidemias de CoV es baja, la mayor frecuencia de infectados por SARS-CoV-2 podría justificar el paso del virus y la posibilidad de clínica neurológica precoz o tardía con mayor incidencia. El seguimiento de los pacientes de la epidemia debe atender con cuidado a la evaluación del SNC.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Introduction</title><p>There is growing evidence that SARS-CoV-2 can gain access to the central nervous system (CNS). We revise the literature on coronavirus infection of the CNS associated with neurological diseases.</p></sec><sec><title>Development</title><p>Neurological symptoms were rarely reported in the SARS-CoV and MERS-CoV epidemics, although isolated cases were described. There are also reports of cases of neurological symptoms associated with CoV-OC43 and CoV-229E infection. The presence of neurological lesions, especially demyelinating lesions in the mouse hepatitis virus model, may explain the mechanisms by which coronaviruses enter the CNS, particularly those related with the immune response. This may explain the presence of coronavirus in patients with multiple sclerosis. We review the specific characteristics of SARS-CoV-2 and address the question of whether the high number of cases may be associated with greater CNS involvement.</p></sec><sec><title>Conclusion</title><p>Although neurological symptoms are not frequent in coronavirus epidemics, the high number of patients with SARS-CoV-2 infection may explain the presence of the virus in the CNS and increase the likelihood of early- or delayed-onset neurological symptoms. Follow-up of patients affected by the SARS-CoV-2 epidemic should include careful assessment of the CNS.</p></sec></trans-abstract><kwd-group id="kwd0005"><title>Palabras clave</title><kwd>Coronavirus</kwd><kwd>SARS-CoV</kwd><kwd>MERS-CoV</kwd><kwd>Esclerosis múltiple</kwd><kwd>SARS-CoV-2</kwd><kwd>Virus murino de la hepatitis</kwd><kwd>Síntomas neurológicos</kwd><kwd>Sistema nervioso central</kwd></kwd-group><kwd-group xml:lang="en" id="kwd0010"><title>Keywords</title><kwd>Coronavirus</kwd><kwd>SARS-CoV</kwd><kwd>MERS-CoV</kwd><kwd>Multiple sclerosis</kwd><kwd>SARS-CoV-2</kwd><kwd>Mouse hepatitis virus</kwd><kwd>Neurological symptoms</kwd><kwd>Central nervous system</kwd></kwd-group></article-meta></front><body><p id="par0005">La asociación a coronavirus que infectaban a humanos estaba asociada a enfermedades menores del sistema respiratorio superior e inferior tanto en niños como en adultos. Los 4 coronavirus humanos endémicos 229E-CoV, NL63-CoV, OC43-CoV y HKU1-CoV han estado considerados entre las causas del resfriado común. Dos de ellos están considerados como αCoV (229E-CoV y NL63-CoV) y 2 de ellos como βCoV (OC43-CoV y HKU1-CoV)<xref rid="bib0450" ref-type="bibr"><sup>1</sup></xref>. Dos nuevos coronavirus, también βCoV (SARS-CoV y MERS-CoV9) se han comportado de forma mucho más agresiva, en forma de epidemias con pacientes que presentaron manifestaciones extrapulmonares e incluso muerte. Así, en 2003, SARS-CoV fue identificado como la causa de un cuadro respiratorio grave que apareció por primera vez en la provincia de Guangdong, China, y más tarde, en 2004, MERS-CoV fue el responsable de una epidemia que tuvo su mayor impacto en la Península Arábica. El 31 de diciembre de 2019, la OMS comunica de casos de neumonía en la ciudad de Wuhan, provincia de Hubei, China, en que se demuestra la presencia de un nuevo CoV, 2019-nCoV (SARS-CoV-2), cuya difusión se realiza rápidamente en China y en el resto del mundo, y que se encuentra dentro de las características del β-CoV, con una similitud bastante amplia a SARS-CoV. La pandemia por SARS-CoV-2 está llegando a todo el mundo, con una amplia mortalidad y un amplio impacto social que vivimos en la actualidad, y que probablemente acabará afectando a un gran número de personas.</p><p id="par0010">El sistema nervioso central (SNC) es vulnerable a los virus, y muchos de ellos acaban llegando al cerebro como el virus del herpes<xref rid="bib0455" ref-type="bibr"><sup>2</sup></xref>, los arbovirus<xref rid="bib0460" ref-type="bibr"><sup>3</sup></xref>, el sarampión<xref rid="bib0465" ref-type="bibr"><sup>4</sup></xref>, la influenza y el VIH<xref rid="bib0470" ref-type="bibr"><sup>5</sup></xref>, entre otros. Los coronavirus también pueden actuar sobre el SNC<xref rid="bib0475" ref-type="bibr">6</xref>, <xref rid="bib0480" ref-type="bibr">7</xref>, y en consecuencia una pandemia con un número tan alto de afectados podría suponer la aparición de cuadros neurológicos. La presente revisión pretende analizar la información existe sobre la acción de los coronavirus humanos en el SNC.</p><sec id="sec0005"><title>Cuadro neurológicos por coronavirus</title><p id="par0015">Es indudable que los CoV penetran en el SNC. Se han detectado RNA de CoV en el sistema nervioso central de pacientes con diversas enfermedades neurológicas<xref rid="bib0485" ref-type="bibr">8</xref>, <xref rid="bib0490" ref-type="bibr">9</xref>, y ello ha tenido una traducción clínica en cuadros encefalíticos en niños<xref rid="bib0495" ref-type="bibr"><sup>10</sup></xref> y también se han observado meningitis, y en el síndrome de Guillain-Barré u otras enfermedades de base neuroinmunitaria<xref rid="bib0500" ref-type="bibr">11</xref>, <xref rid="bib0505" ref-type="bibr">12</xref>, <xref rid="bib0510" ref-type="bibr">13</xref>, <xref rid="bib0515" ref-type="bibr">14</xref>, <xref rid="bib0520" ref-type="bibr">15</xref>. Asimismo, se han observado en el contexto de infecciones por CoV<xref rid="bib0525" ref-type="bibr">16</xref>, <xref rid="bib0530" ref-type="bibr">17</xref>. Entre los CoV, OC43-CoV ha sido considerado como un virus con mayor capacidad neuroinvasiva, ya que se ha demostrado que invade, se propaga y persiste dentro del SNC en el ratón, afectando directamente a los neuronas<xref rid="bib0535" ref-type="bibr">18</xref>, <xref rid="bib0540" ref-type="bibr">19</xref> y se ha descrito que utiliza el transporte axonal para su difusión<xref rid="bib0545" ref-type="bibr"><sup>20</sup></xref>. OC43-CoV tiene la capacidad de inducir degeneración y muerte celular<xref rid="bib0550" ref-type="bibr">21</xref>, <xref rid="bib0555" ref-type="bibr">22</xref>, <xref rid="bib0560" ref-type="bibr">23</xref>. En el humano se ha detectado este virus en muestras del cerebro humano de pacientes que padecen enfermedades neurológicas como Alzheimer, enfermedad de Parkinson y esclerosis múltiple (EM), y en sanos. Asimismo, se ha asociado de forma similar a 229E-CoV a la presencia de convulsiones febriles<xref rid="bib0565" ref-type="bibr"><sup>24</sup></xref>. Además, OC43-CoV fue detectado en el cerebro de un niño inmunodeficiente que murió de encefalitis<xref rid="bib0570" ref-type="bibr"><sup>25</sup></xref>. Ambos virus, OC43-CoV y 229E-CoV tienen la capacidad de entrar en las células de la inmunidad innata<xref rid="bib0575" ref-type="bibr">26</xref>, <xref rid="bib0580" ref-type="bibr">27</xref>.</p></sec><sec id="sec0010"><title>MERS-CoV y SARS-CoV</title><p id="par0020">SARS-CoV y el MERS-CoV pueden causar una infección grave del tracto respiratorio inferior con síndrome de dificultad respiratoria aguda y manifestaciones extrapulmonares como diarrea, linfopenia, pruebas de función hepática y renal alteradas, y síndrome de disfunción multiorgánica, tanto entre huéspedes inmunocompetentes como inmunocomprometidos con tasas de mortalidad superior al 10%, aunque existen casos asintomáticos<xref rid="bib0585" ref-type="bibr"><sup>28</sup></xref>. Ambos virus han sido responsables de 2 epidemias con un número alto de personas contagiadas. La presencia de cuadros neurológicos no ha sido alta en los diferentes estudios, aunque todos ellos analizan la fase inicial de la epidemia. Un estudio retrospectivo en Arabia Saudita se encontró que el 25,7% de los pacientes con MERS desarrollaron confusión y el 8,6% experimentó convulsiones<xref rid="bib0590" ref-type="bibr"><sup>29</sup></xref>. Solo 4 casos con afectación del SNC (encefalomielitis diseminada aguda, accidente cerebrovascular y encefalitis) y un caso con polineuropatía de enfermedad crítica ha sido reportado para pacientes con MERS<xref rid="bib0595" ref-type="bibr">30</xref>, <xref rid="bib0600" ref-type="bibr">31</xref>. También se ha descrito la presencia síndrome de Guillain-Barré y neuropatía periférica de aparición tardía, y en algún paciente se describe el cronograma entre la presencia del cuadro infeccioso y el neurológico<xref rid="bib0605" ref-type="bibr"><sup>32</sup></xref>. Existe un caso descrito asociado a una hemorragia cerebral en la que los autores consideran que el paciente no tenía riesgo de presentar el cuadro por otro origen<xref rid="bib0610" ref-type="bibr"><sup>33</sup></xref>. Un estudio <italic>in vitro</italic> ha observado que MERS-CoV tiene una especial sensibilidad para invadir diversas líneas celulares específicas y halla que entre ellas muestra la capacidad de infectar células neuronales humanas<xref rid="bib0615" ref-type="bibr"><sup>34</sup></xref>. La cuestión de que las complicaciones neurológicas halladas con MERS-CoV son de aparición tardía, la ausencia del virus en el LCR y la presencia de cuadros de síndrome de Guillain-Barré no está aclarado y puede estar relacionada con la respuesta inmune<xref rid="bib0620" ref-type="bibr"><sup>35</sup></xref>. Algunos autores han señalado que la falta de hallazgos del virus en muestras biológicas puede ser debido a cuestiones metodológicas<xref rid="bib0625" ref-type="bibr"><sup>36</sup></xref>. Durante el brote por SARS-CoV en 2002-2003, la descripción de cuadros neurológicos fue baja<xref rid="bib0630" ref-type="bibr"><sup>37</sup></xref> y con casos aislados<xref rid="bib0635" ref-type="bibr"><sup>38</sup></xref>. Seis pacientes que desarrollaron polineuropatía axonal al mes después del inicio del SARS mejoraron en el seguimiento. También hubo pacientes que experimentaron alteraciones neuromusculares<xref rid="bib0640" ref-type="bibr"><sup>39</sup></xref> como miopatía<xref rid="bib0645" ref-type="bibr"><sup>40</sup></xref> y rabdomiólisis. SARS fue un cuadro más grave<xref rid="bib0650" ref-type="bibr"><sup>41</sup></xref>, de forma que se ha sugerido que estas alteraciones musculares podrían ser debidas más a la situación crítica de los pacientes que al propio virus. Se describieron también la presencia de ictus<xref rid="bib0655" ref-type="bibr">42</xref>, <xref rid="bib0660" ref-type="bibr">43</xref>.</p></sec><sec id="sec0015"><title>Coronavirus y esclerosis múltiple</title><p id="par0025">Los CoV han sido propuestos como una hipótesis de asociación ambiental a la EM<xref rid="bib0665" ref-type="bibr"><sup>44</sup></xref>. Ello ha sido apoyado por varios argumentos. Se han detectado partículas similares a coronavirus en el tejido cerebral autopsiado de un paciente con EM<xref rid="bib0670" ref-type="bibr"><sup>45</sup></xref>. CoV se han aislado en el cerebro obtenido en la autopsia de 2 pacientes con EM<xref rid="bib0675" ref-type="bibr"><sup>46</sup></xref> y se ha obtenido RNA en el cerebro de otros pacientes<xref rid="bib0680" ref-type="bibr">47</xref>, <xref rid="bib0685" ref-type="bibr">48</xref>, <xref rid="bib0690" ref-type="bibr">49</xref>. Se ha observado la síntesis intratecal de anticuerpos anti-CoV humanos indicativos de una infección del SNC en pacientes con EM<xref rid="bib0695" ref-type="bibr"><sup>50</sup></xref>. Se ha detectado RNA de CoV humanos. Se ha hallado RNA de CoV humanos en el LCR de pacientes con EM<xref rid="bib0700" ref-type="bibr"><sup>51</sup></xref>. Desde el punto de vista experimental se ha demostrado que CoV humanos pueden infectar neuronas, astrocitos y microglía en cultivos primarios<xref rid="bib0705" ref-type="bibr"><sup>52</sup></xref>, y también a células gliales humanas inmortalizadas<xref rid="bib0710" ref-type="bibr"><sup>53</sup></xref>. Es interesante que CoV humanos pueden infectar células de estirpe oligodendrocitaria y oligodendrocios<xref rid="bib0715" ref-type="bibr"><sup>54</sup></xref>. Asimismo, ha reforzado esta hipótesis el hecho que las infecciones de las vías respiratorias superiores de origen viral que pueden estar relacionadas con CoV humanos son un desencadenante importante de los brotes de EM<xref rid="bib0720" ref-type="bibr">55</xref>, <xref rid="bib0725" ref-type="bibr">56</xref>.</p></sec><sec id="sec0020"><title>El virus de la hepatitis de ratón</title><p id="par0030">El MHV-CoA es un virus que afecta al ratón<xref rid="bib0730" ref-type="bibr"><sup>57</sup></xref> y no al humano que induce trastornos neurológicos<xref rid="bib0735" ref-type="bibr">58</xref>, <xref rid="bib0740" ref-type="bibr">59</xref>, y ello ha posibilitado la creación de un modelo experimental para estudiar el papel de los CoV en el SNC. Las cepas neurotrópicas de MHV pueden invadir el SNC por inoculación intranasal en ratones<xref rid="bib0745" ref-type="bibr"><sup>60</sup></xref> y también por vía sanguínea, y ello se ha observado también en primates<xref rid="bib0750" ref-type="bibr"><sup>61</sup></xref>. El paso por la barrera hematoencefalica se ha relacionado con la producción de interferón-beta por las células epiteliales de la microcirculación cerebral<xref rid="bib0755" ref-type="bibr"><sup>62</sup></xref>. La infección por MHV-CoV desencadena una encefalomielitis aguda asociada con áreas focales de desmielinización, y se ha analizado el papel de la respuesta inmune en su evolución<xref rid="bib0760" ref-type="bibr"><sup>63</sup></xref>. La activación de la microglía, la descarga de mediadores inflamatorios generarían un microambiente local del SNC que influiría en la replicación viral y lo que puede conducir a la desmielinización<xref rid="bib0765" ref-type="bibr"><sup>64</sup></xref>. Es por ello, que la aparición de lesiones desmielinizantes ha sugerido que este modelo podría ser aplicable al conocimiento de la EM.</p></sec><sec id="sec0025"><title>La epidemia de SARS-CoV-2 y la posibilidad de que el cerebro pueda ser reservorio del virus</title><p id="par0035">Aunque se asemeje, el nuevo virus es distinto a SARS-Cov<xref rid="bib0770" ref-type="bibr"><sup>65</sup></xref>, causante de la epidemia actual presenta diferencias genéticas y estructurales con los anteriores, y forma parte del grupo βCoV. Una de las características de este nuevo virus es que es altamente difundible<xref rid="bib0775" ref-type="bibr"><sup>66</sup></xref> y en mayor medida que SARS-CoV<xref rid="bib0780" ref-type="bibr"><sup>67</sup></xref>, propagado por gotas, contacto directo y contacto con objetos infectados, y que se propaga también con personas infectadas asintomáticos<xref rid="bib0785" ref-type="bibr">68</xref>, <xref rid="bib0790" ref-type="bibr">69</xref>, <xref rid="bib0795" ref-type="bibr">70</xref>. Aunque existen distintos estudios observacionales que han analizado los síntomas de la enfermedad, la presencia de síntomas neurológicos es baja, salvo cefalea y cuadros vestibulares en estudios observaciones<xref rid="bib0800" ref-type="bibr">71</xref>, <xref rid="bib0805" ref-type="bibr">72</xref>, <xref rid="bib0810" ref-type="bibr">73</xref>, <xref rid="bib0815" ref-type="bibr">74</xref>, <xref rid="bib0820" ref-type="bibr">75</xref>, <xref rid="bib0825" ref-type="bibr">76</xref>, y en un estudio específico en pacientes hospitalizados<xref rid="bib0830" ref-type="bibr"><sup>77</sup></xref> o casos aislados<xref rid="bib0835" ref-type="bibr"><sup>78</sup></xref> a pesar que algunos autores han señalado de la posibilidad de que el virus pueda afectar al sistema nervioso central como en SARS-CoV en el que el virus se halló en el cerebro de pacientes<xref rid="bib0840" ref-type="bibr"><sup>79</sup></xref>. Algunos datos clínicos parecen apuntar a unas características diferenciales como las alteraciones olfatorias, descrita por grupos alemanes por primera vez, y la presencia de alucinaciones que no han sido referidas por SARS-CoV ni MERS-CoV. El virus tiene algunas características que han apoyado que tenga una especial sensibilidad hacia el SNC.</p><p id="par0040">Las principales diferencias estructurales entre SARS-CoV y SARS-CoV-2 está en la proteína de fusión y en las proteínas accesorias ORF3b y ORF8. El genoma del virus codifica 4 proteínas estructurales principales, incluidas la espiga (S), la nucleocápside, la membrana y la envoltura que se requieren para formar la partícula viral completa<xref rid="bib0845" ref-type="bibr"><sup>80</sup></xref>. Una glicoproteína de la proteína S puede ser un desencadenante de enfermedades neurodegenerativas<xref rid="bib0850" ref-type="bibr"><sup>81</sup></xref>. Al ingresar a las células huésped, el genoma viral se traduce en 2 poliproteínas precursoras grandes que se procesan en 16 proteínas no estructurales maduras (NSP1-NSP16) mediante proteinasas virales codificadas por ORF1a, entre otras. Estas nspS realizan una función crucial durante la replicación y transcripción del ARN viral<xref rid="bib0855" ref-type="bibr"><sup>82</sup></xref>, y ORF3b se ha relacionado con la respuesta inmune<xref rid="bib0860" ref-type="bibr"><sup>83</sup></xref>. La subunidad 1 de la proteína de fusión se une también al receptor ACE2 como SARS-CoV, que es el lugar de enlace con el huésped y que ha planteado la posibilidad de crear un modelo experimental para la infección<xref rid="bib0865" ref-type="bibr"><sup>84</sup></xref>. Un hecho relevante es que el cerebro tiene una expresión alta de receptores de ACE2<xref rid="bib0870" ref-type="bibr"><sup>85</sup></xref>, lo que ha sugerido que por esta razón en esta epidemia la penetración del virus al SNC puede ser alta<xref rid="bib0875" ref-type="bibr"><sup>86</sup></xref>. Estudios previos demostraron la correlación positiva de la expresión de ACE2 y la infección de SARS-CoV <italic>in vitro</italic><xref rid="bib0880" ref-type="bibr"><sup>87</sup></xref>. Los virus pueden acceder al SNC por 2 vías, la hematógena, un virus infectará las células endoteliales de la barrera hematoencefálica y la neuronal, aunque también podría diseminarse localmente a través de la placa cribiforme del hueso etmoides Sin embargo, cruzar la barrera hematoencefálica<xref rid="bib0885" ref-type="bibr"><sup>88</sup></xref> es poco probable por el SARS-CoV-2 debido al tamaño de este virus, por lo que es más probable que acceda a través del nervio olfatorio o del trigémino, de manera que la frecuencia de alteraciones olfatorias en la epidemia podría ser un indicación de penetración en el SNC. En el modelo de MHV-CoV, así como el hallazgo de CoV en el cerebro de pacientes puede sugerir que el virus pueda persistir durante períodos prolongados sin ninguna enfermedad neurológica aparente y el cerebro podría ser un reservorio de virus<xref rid="bib0890" ref-type="bibr"><sup>89</sup></xref>.</p></sec><sec id="sec0030"><title>Conclusión</title><p id="par0045">Los CoV son virus que pueden penetrar en el SNC y generar daño, así como mantenerse en él como reservorio. Aunque la presencia de síntomas neurológicos es baja, su existencia puede justificar el paso del virus y la posibilidad de clínica neurológica precoz o tardía con mayor incidencia. En este sentido, los potenciales cuadros neurológicos que podrían hallarse podrían agruparse en los siguientes: 1) Cuadros asociados a las consecuencias del cuadro infeccioso como el ictus isquémico, aunque la presencia de hemorragia cerebral podría asociarse a la acción del virus sobre el receptor de ACE2; 2) Cuadros asociados a enfermedades oportunistas como se ha observado en las otras epidemias; 3) Cuadros neurológicos asociados al paciente crítico, en aquellos que ingresan en las unidades de intensivos, específicamente alteraciones musculares o rabdomiólisis; 4) Cuadros asociados a la invasión del virus en territorios neurógenos o musculares como las alteraciones olfatorias (olfato y gusto) o miositis y 5) Cuadros no clasificables todavía debido a la falta de información como son las alucinaciones. 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