Neuroinvasive and Neurotropic Human Respiratory Coronaviruses: Potential Neurovirulent Agents in Humans
Identifieur interne : 000876 ( Pmc/Checkpoint ); précédent : 000875; suivant : 000877Neuroinvasive and Neurotropic Human Respiratory Coronaviruses: Potential Neurovirulent Agents in Humans
Auteurs :Source :
- Infectious Diseases and Nanomedicine I ; 2014.
Abstract
In humans, viral infections of the respiratory tract are a leading cause of morbidity and mortality worldwide. Several recognized respiratory viral agents have a neuroinvasive capacity since they can spread from the respiratory tract to the central nervous system (CNS). Once there, infection of CNS cells (neurotropism) could lead to human health problems, such as encephalitis and long-term neurological diseases. Among the various respiratory viruses, coronaviruses are important pathogens of humans and animals. Human Coronaviruses (HCoV) usually infect the upper respiratory tract, where they are mainly associated with common colds. However, in more vulnerable populations, such as newborns, infants, the elderly, and immune-compromised individuals, they can also affect the lower respiratory tract, leading to pneumonia, exacerbations of asthma, respiratory distress syndrome, or even severe acute respiratory syndrome (SARS). The respiratory involvement of HCoV has been clearly established since the 1960s. In addition, for almost three decades now, the scientific literature has also demonstrated that HCoV are neuroinvasive and neurotropic and could induce an overactivation of the immune system, in part by participating in the activation of autoreactive immune cells that could be associated with autoimmunity in susceptible individuals. Furthermore, it was shown that in the murine CNS, neurons are the main target of infection, which causes these essential cells to undergo degeneration and eventually die by some form of programmed cell death after virus infection. Moreover, it appears that the viral surface glycoprotein (S) represents an important factor in the neurodegenerative process. Given all these properties, it has been suggested that these recognized human respiratory pathogens could be associated with the triggering or the exacerbation of neurological diseases for which the etiology remains unknown or poorly understood.
Url:
DOI: 10.1007/978-81-322-1777-0_6
PubMed: 24619619
PubMed Central: 7121612
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neuroinvasive and Neurotropic Human Respiratory Coronaviruses: Potential Neurovirulent Agents in Humans</title></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24619619</idno><idno type="pmc">7121612</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7121612</idno><idno type="RBID">PMC:7121612</idno><idno type="doi">10.1007/978-81-322-1777-0_6</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000171</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000171</idno><idno type="wicri:Area/Pmc/Curation">000171</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000171</idno><idno type="wicri:Area/Pmc/Checkpoint">000876</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000876</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Neuroinvasive and Neurotropic Human Respiratory Coronaviruses: Potential Neurovirulent Agents in Humans</title></analytic><series><title level="j">Infectious Diseases and Nanomedicine I</title><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>In humans, viral infections of the respiratory tract are a leading cause of morbidity and mortality worldwide. Several recognized respiratory viral agents have a neuroinvasive capacity since they can spread from the respiratory tract to the central nervous system (CNS). Once there, infection of CNS cells (neurotropism) could lead to human health problems, such as encephalitis and long-term neurological diseases. Among the various respiratory viruses, coronaviruses are important pathogens of humans and animals. Human Coronaviruses (HCoV) usually infect the upper respiratory tract, where they are mainly associated with common colds. However, in more vulnerable populations, such as newborns, infants, the elderly, and immune-compromised individuals, they can also affect the lower respiratory tract, leading to pneumonia, exacerbations of asthma, respiratory distress syndrome, or even severe acute respiratory syndrome (SARS). The respiratory involvement of HCoV has been clearly established since the 1960s. In addition, for almost three decades now, the scientific literature has also demonstrated that HCoV are neuroinvasive and neurotropic and could induce an overactivation of the immune system, in part by participating in the activation of autoreactive immune cells that could be associated with autoimmunity in susceptible individuals. Furthermore, it was shown that in the murine CNS, neurons are the main target of infection, which causes these essential cells to undergo degeneration and eventually die by some form of programmed cell death after virus infection. Moreover, it appears that the viral surface glycoprotein (S) represents an important factor in the neurodegenerative process. Given all these properties, it has been suggested that these recognized human respiratory pathogens could be associated with the triggering or the exacerbation of neurological diseases for which the etiology remains unknown or poorly understood.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Vareille, M" uniqKey="Vareille M">M Vareille</name></author><author><name sortKey="Kieninger, E" uniqKey="Kieninger E">E Kieninger</name></author><author><name sortKey="Edwards, Mr" uniqKey="Edwards M">MR Edwards</name></author><author><name sortKey="Regamey, N" uniqKey="Regamey N">N Regamey</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jartti, T" uniqKey="Jartti T">T Jartti</name></author><author><name sortKey="Jartti, L" uniqKey="Jartti L">L Jartti</name></author><author><name sortKey="Ruuskanen, O" uniqKey="Ruuskanen O">O Ruuskanen</name></author><author><name sortKey="Soderlund Venermo, M" 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<front><journal-meta><journal-id journal-id-type="publisher-id">978-81-322-1777-0</journal-id><journal-id journal-id-type="doi">10.1007/978-81-322-1777-0</journal-id><journal-id journal-id-type="nlm-ta">Infectious Diseases and Nanomedicine I</journal-id><journal-title-group><journal-title>Infectious Diseases and Nanomedicine I</journal-title><journal-subtitle>First International Conference (ICIDN – 2012), Dec. 15-18, 2012, Kathmandu, Nepal</journal-subtitle></journal-title-group><isbn publication-format="print">978-81-322-1776-3</isbn><isbn publication-format="electronic">978-81-322-1777-0</isbn></journal-meta><article-meta><article-id pub-id-type="pmid">24619619</article-id><article-id pub-id-type="pmc">7121612</article-id><article-id pub-id-type="publisher-id">6</article-id><article-id pub-id-type="doi">10.1007/978-81-322-1777-0_6</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Neuroinvasive and Neurotropic Human Respiratory Coronaviruses: Potential Neurovirulent Agents in Humans</article-title></title-group><contrib-group content-type="book editors"><contrib contrib-type="editor"><name><surname>Adhikari</surname><given-names>Rameshwar</given-names></name><address><email>nepalpolymer@yahoo.com</email></address><xref ref-type="aff" rid="Aff5">5</xref></contrib><contrib contrib-type="editor"><name><surname>Thapa</surname><given-names>Santosh</given-names></name><address><phone>3258</phone><email>icidn2012@gmail.com</email></address><xref ref-type="aff" rid="Aff6">6</xref></contrib><aff id="Aff5"><label>5</label><institution-wrap><institution-id institution-id-type="GRID">grid.80817.36</institution-id><institution-id institution-id-type="ISNI">0000000121146728</institution-id><institution>Central Department of Chemistry,</institution><institution>Tribhuvan University,</institution></institution-wrap>Kathmandu, Nepal</aff><aff id="Aff6"><label>6</label><institution-wrap><institution-id institution-id-type="GRID">grid.80817.36</institution-id><institution-id institution-id-type="ISNI">0000000121146728</institution-id><institution>Department of Microbiology,</institution><institution>Tribhuvan University,</institution></institution-wrap>Kathmandu, Nepal</aff></contrib-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Desforges</surname><given-names>Marc</given-names></name><address><email>marc.desforges@iaf.inrs.ca</email></address><xref ref-type="aff" rid="Aff7"></xref></contrib><contrib contrib-type="author"><name><surname>Le Coupanec</surname><given-names>Alain</given-names></name><xref ref-type="aff" rid="Aff7"></xref></contrib><contrib contrib-type="author"><name><surname>Brison</surname><given-names>Élodie</given-names></name><xref ref-type="aff" rid="Aff7"></xref></contrib><contrib contrib-type="author"><name><surname>Meessen-Pinard</surname><given-names>Mathieu</given-names></name><xref ref-type="aff" rid="Aff7"></xref></contrib><contrib contrib-type="author"><name><surname>Talbot</surname><given-names>Pierre J.</given-names></name><address><email>pierre.talbot@iaf.inrs.ca</email></address><xref ref-type="aff" rid="Aff7"></xref></contrib><aff id="Aff7"><institution-wrap><institution-id institution-id-type="GRID">grid.265695.b</institution-id><institution>Laboratory of Neuroimmunovirology, INRS-Institut Armand-Frappier, Institut national de la recherche scientifique,</institution><institution>Université du Québec,</institution></institution-wrap>531 boulevard des Prairies, Laval, QC H7V IB7 Canada</aff></contrib-group><pub-date pub-type="epub"><day>12</day><month>3</month><year>2014</year></pub-date><pub-date pub-type="collection"><year>2014</year></pub-date><volume>807</volume><fpage>75</fpage><lpage>96</lpage><permissions><copyright-statement>© Springer India 2014</copyright-statement><license><license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p></license></permissions><abstract id="Abs1"><p>In humans, viral infections of the respiratory tract are a leading cause of morbidity and mortality worldwide. Several recognized respiratory viral agents have a neuroinvasive capacity since they can spread from the respiratory tract to the central nervous system (CNS). Once there, infection of CNS cells (neurotropism) could lead to human health problems, such as encephalitis and long-term neurological diseases. Among the various respiratory viruses, coronaviruses are important pathogens of humans and animals. Human Coronaviruses (HCoV) usually infect the upper respiratory tract, where they are mainly associated with common colds. However, in more vulnerable populations, such as newborns, infants, the elderly, and immune-compromised individuals, they can also affect the lower respiratory tract, leading to pneumonia, exacerbations of asthma, respiratory distress syndrome, or even severe acute respiratory syndrome (SARS). The respiratory involvement of HCoV has been clearly established since the 1960s. In addition, for almost three decades now, the scientific literature has also demonstrated that HCoV are neuroinvasive and neurotropic and could induce an overactivation of the immune system, in part by participating in the activation of autoreactive immune cells that could be associated with autoimmunity in susceptible individuals. Furthermore, it was shown that in the murine CNS, neurons are the main target of infection, which causes these essential cells to undergo degeneration and eventually die by some form of programmed cell death after virus infection. Moreover, it appears that the viral surface glycoprotein (S) represents an important factor in the neurodegenerative process. Given all these properties, it has been suggested that these recognized human respiratory pathogens could be associated with the triggering or the exacerbation of neurological diseases for which the etiology remains unknown or poorly understood.</p></abstract><kwd-group xml:lang="en"><title>Keywords</title><kwd>Respiratory viral infection</kwd><kwd>Coronavirus</kwd><kwd>Neuroinvasion</kwd><kwd>CNS infection</kwd><kwd>Neurological diseases</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© Springer India 2014</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc><affiliations><list></list><tree></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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