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Molecular pathology of emerging coronavirus infections

Identifieur interne : 001006 ( Pmc/Checkpoint ); précédent : 001005; suivant : 001007

Molecular pathology of emerging coronavirus infections

Auteurs : Lisa E. Gralinski [États-Unis] ; Ralph S. Baric [États-Unis]

Source :

RBID : PMC:4267971

Abstract

Respiratory viruses can cause a wide spectrum of pulmonary diseases, ranging from mild, upper respiratory tract infections to severe and life-threatening lower respiratory tract infections, including the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Viral clearance and subsequent recovery from infection require activation of an effective host immune response; however, many immune effector cells may also cause injury to host tissues. Severe acute respiratory syndrome (SARS) coronavirus and Middle East respiratory syndrome (MERS) coronavirus cause severe infection of the lower respiratory tract, with 10% and 35% overall mortality rates, respectively; however, >50% mortality rates are seen in the aged and immunosuppressed populations. While these viruses are susceptible to interferon treatment in vitro, they both encode numerous genes that allow for successful evasion of the host immune system until after high virus titres have been achieved. In this review, we discuss the importance of the innate immune response and the development of lung pathology following human coronavirus infection.


Url:
DOI: 10.1002/path.4454
PubMed: 25270030
PubMed Central: 4267971


Affiliations:


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PMC:4267971

Le document en format XML

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</TEI>
<pmc article-type="research-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">J Pathol</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Pathol</journal-id>
<journal-id journal-id-type="publisher-id">path</journal-id>
<journal-title-group>
<journal-title>The Journal of Pathology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0022-3417</issn>
<issn pub-type="epub">1096-9896</issn>
<publisher>
<publisher-name>John Wiley & Sons, Ltd</publisher-name>
<publisher-loc>Chichester, UK</publisher-loc>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">25270030</article-id>
<article-id pub-id-type="pmc">4267971</article-id>
<article-id pub-id-type="doi">10.1002/path.4454</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Invited Reviews</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Molecular pathology of emerging coronavirus infections</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Gralinski</surname>
<given-names>Lisa E</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Baric</surname>
<given-names>Ralph S</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
<xref ref-type="aff" rid="au2">2</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
<aff id="au1">
<label>1</label>
<institution>Department of Epidemiology, University of North Carolina</institution>
<addr-line>Chapel Hill, NC, USA</addr-line>
</aff>
<aff id="au2">
<label>2</label>
<institution>Department of Microbiology and Immunology, University of North Carolina</institution>
<addr-line>Chapel Hill, NC, USA</addr-line>
</aff>
</contrib-group>
<author-notes>
<corresp id="cor1">*Correspondence to: RS Baric, Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599–7435, USA. E-mail:
<email>rbaric@email.unc.ed</email>
</corresp>
<fn>
<p>No conflicts of interest were declared.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub">
<month>1</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub">
<day>11</day>
<month>12</month>
<year>2014</year>
</pub-date>
<volume>235</volume>
<issue>2</issue>
<fpage>185</fpage>
<lpage>195</lpage>
<history>
<date date-type="received">
<day>18</day>
<month>9</month>
<year>2014</year>
</date>
<date date-type="accepted">
<day>25</day>
<month>9</month>
<year>2014</year>
</date>
</history>
<permissions>
<copyright-statement>© 2014 The Authors.
<italic>The Journal of Pathology</italic>
published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.</copyright-statement>
<copyright-year>2014</copyright-year>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc-nd/3.0/">
<license-p>This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.</license-p>
</license>
</permissions>
<abstract>
<p>Respiratory viruses can cause a wide spectrum of pulmonary diseases, ranging from mild, upper respiratory tract infections to severe and life-threatening lower respiratory tract infections, including the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Viral clearance and subsequent recovery from infection require activation of an effective host immune response; however, many immune effector cells may also cause injury to host tissues. Severe acute respiratory syndrome (SARS) coronavirus and Middle East respiratory syndrome (MERS) coronavirus cause severe infection of the lower respiratory tract, with 10% and 35% overall mortality rates, respectively; however, >50% mortality rates are seen in the aged and immunosuppressed populations. While these viruses are susceptible to interferon treatment
<italic>in vitro</italic>
, they both encode numerous genes that allow for successful evasion of the host immune system until after high virus titres have been achieved. In this review, we discuss the importance of the innate immune response and the development of lung pathology following human coronavirus infection.</p>
</abstract>
<kwd-group>
<kwd>SARS-CoV</kwd>
<kwd>MERS-CoV</kwd>
<kwd>coronavirus</kwd>
<kwd>acute respiratory distress syndrome</kwd>
<kwd>ARDS</kwd>
<kwd>acute lung injury</kwd>
<kwd>type II pneumocytes</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
<affiliations>
<list>
<country>
<li>États-Unis</li>
</country>
<region>
<li>Caroline du Nord</li>
</region>
</list>
<tree>
<country name="États-Unis">
<region name="Caroline du Nord">
<name sortKey="Gralinski, Lisa E" sort="Gralinski, Lisa E" uniqKey="Gralinski L" first="Lisa E" last="Gralinski">Lisa E. Gralinski</name>
</region>
<name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S" last="Baric">Ralph S. Baric</name>
<name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S" last="Baric">Ralph S. Baric</name>
</country>
</tree>
</affiliations>
</record>

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