Use of Toll-Like Receptor 3 Agonists Against Respiratory Viral Infections
Identifieur interne : 001393 ( Ncbi/Merge ); précédent : 001392; suivant : 001394Use of Toll-Like Receptor 3 Agonists Against Respiratory Viral Infections
Auteurs : Me Christopher ; Jp WongSource :
- Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry [ 1871-5230 ] ; 2011.
Abstract
Respiratory RNA viruses are constantly evolving, thus requiring development of additional prophylactic and therapeutic strategies. Harnessing the innate immune system to non-specifically respond to viral infection has the advantage of being able to circumvent viral mutations that render the virus resistant to a particular therapeutic agent. Viruses are recognized by various cellular receptors, including Toll-like receptor (TLR) 3 which recognizes double-stranded (ds)RNA produced during the viral replication cycle. TLR3 agonists include synthetic dsRNA such as poly (IC), poly (ICLC) and poly (AU). These agents have been evaluated and found to be effective against a number of viral agents. One major limitation has been the toxicity associated with administration of these drugs. Significant time and effort have been spent to develop alternatives/modifications that will minimize these adverse effects. This review will focus on the TLR3 agonist, poly (IC)/(ICLC) with respect to its use in treatment/prevention of respiratory viral infections.
Url:
DOI: 10.2174/187152111800194434
PubMed: NONE
PubMed Central: 3552307
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Use of Toll-Like Receptor 3 Agonists Against Respiratory Viral Infections</title><author><name sortKey="Christopher, Me" sort="Christopher, Me" uniqKey="Christopher M" first="Me" last="Christopher">Me Christopher</name></author><author><name sortKey="Wong, Jp" sort="Wong, Jp" uniqKey="Wong J" first="Jp" last="Wong">Jp Wong</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmc">3552307</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552307</idno><idno type="RBID">PMC:3552307</idno><idno type="doi">10.2174/187152111800194434</idno><idno type="pmid">NONE</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">000901</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000901</idno><idno type="wicri:Area/Pmc/Curation">000901</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000901</idno><idno type="wicri:Area/Pmc/Checkpoint">000770</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000770</idno><idno type="wicri:Area/Ncbi/Merge">001393</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Use of Toll-Like Receptor 3 Agonists Against Respiratory Viral Infections</title><author><name sortKey="Christopher, Me" sort="Christopher, Me" uniqKey="Christopher M" first="Me" last="Christopher">Me Christopher</name></author><author><name sortKey="Wong, Jp" sort="Wong, Jp" uniqKey="Wong J" first="Jp" last="Wong">Jp Wong</name></author></analytic><series><title level="j">Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry</title><idno type="ISSN">1871-5230</idno><idno type="eISSN">1875-614X</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Respiratory RNA viruses are constantly evolving, thus requiring development of additional prophylactic and
therapeutic strategies. Harnessing the innate immune system to non-specifically respond to viral infection has the
advantage of being able to circumvent viral mutations that render the virus resistant to a particular therapeutic agent.
Viruses are recognized by various cellular receptors, including Toll-like receptor (TLR) 3 which recognizes double-stranded
(ds)RNA produced during the viral replication cycle. TLR3 agonists include synthetic dsRNA such as poly (IC),
poly (ICLC) and poly (AU). These agents have been evaluated and found to be effective against a number of viral agents.
One major limitation has been the toxicity associated with administration of these drugs. Significant time and effort have
been spent to develop alternatives/modifications that will minimize these adverse effects. This review will focus on the
TLR3 agonist, poly (IC)/(ICLC) with respect to its use in treatment/prevention of respiratory viral infections.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey=" Rogers, B" uniqKey=" Rogers B">B Rogers</name></author><author><name sortKey="Dennison, K" uniqKey="Dennison K">K Dennison</name></author><author><name sortKey="Adepoju, N" uniqKey="Adepoju N">N Adepoju</name></author><author><name sortKey="Dowd, S" uniqKey="Dowd S">S Dowd</name></author><author><name sortKey="Uedoi, K" uniqKey="Uedoi K">K Uedoi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey=" Ruprecht, Rm" uniqKey=" Ruprecht R">RM Ruprecht</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey=" Ashkar, Aa" uniqKey=" Ashkar A">AA Ashkar</name></author><author><name sortKey="Bauer, S" uniqKey="Bauer S">S Bauer</name></author><author><name sortKey="Mitchell, Wj" uniqKey="Mitchell W">WJ 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Antiinflamm Antiallergy Agents Med Chem</journal-id><journal-id journal-id-type="iso-abbrev">Antiinflamm Antiallergy Agents Med Chem</journal-id><journal-id journal-id-type="publisher-id">AIAAMC</journal-id><journal-title-group><journal-title>Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry</journal-title></journal-title-group><issn pub-type="ppub">1871-5230</issn><issn pub-type="epub">1875-614X</issn><publisher><publisher-name>Bentham Science Publishers</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmc">3552307</article-id><article-id pub-id-type="publisher-id">AIAAMC-10-327</article-id><article-id pub-id-type="doi">10.2174/187152111800194434</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Use of Toll-Like Receptor 3 Agonists Against Respiratory Viral Infections</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Christopher</surname><given-names>ME</given-names></name><xref ref-type="corresp" rid="cor1">*</xref></contrib><contrib contrib-type="author"><name><surname>Wong</surname><given-names>JP</given-names></name></contrib></contrib-group><aff>DRDC Suffield, Box 4000, Station Main, Medicine Hat, AB, T1A 8K6, Canada</aff><author-notes><corresp id="cor1"><label>*</label>Address correspondence to this author at the DRDC Suffield, Box 4000, Station Main, Medicine Hat, AB, T1A 8K6, Canada;<email xlink:href="mary.christopher@drdc-rddc.gc.ca">mary.christopher@drdc-rddc.gc.ca</email></corresp></author-notes><pub-date pub-type="ppub"><month>10</month><year>2011</year></pub-date><pub-date pub-type="epub"><month>10</month><year>2011</year></pub-date><volume>10</volume><issue>5</issue><fpage>327</fpage><lpage>338</lpage><history><date date-type="received"><day>15</day><month>11</month><year>2011</year></date><date date-type="rev-recd"><day>30</day><month>11</month><year>2011</year></date><date date-type="accepted"><day>10</day><month>12</month><year>2011</year></date></history><permissions><copyright-statement>© 2011 Bentham Science Publishers</copyright-statement><copyright-year>2011</copyright-year><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/2.5/"><license-p>This is an open access article distributed under the terms of the Creative Commons Attribution License (<uri xlink:type="simple" xlink:href="http://creativecommons.org/licenses/by/2.5/">http://creativecommons.org/licenses/by/2.5/</uri>), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>Respiratory RNA viruses are constantly evolving, thus requiring development of additional prophylactic and
therapeutic strategies. Harnessing the innate immune system to non-specifically respond to viral infection has the
advantage of being able to circumvent viral mutations that render the virus resistant to a particular therapeutic agent.
Viruses are recognized by various cellular receptors, including Toll-like receptor (TLR) 3 which recognizes double-stranded
(ds)RNA produced during the viral replication cycle. TLR3 agonists include synthetic dsRNA such as poly (IC),
poly (ICLC) and poly (AU). These agents have been evaluated and found to be effective against a number of viral agents.
One major limitation has been the toxicity associated with administration of these drugs. Significant time and effort have
been spent to develop alternatives/modifications that will minimize these adverse effects. This review will focus on the
TLR3 agonist, poly (IC)/(ICLC) with respect to its use in treatment/prevention of respiratory viral infections.</p></abstract><kwd-group><title>Keyword:</title><kwd>Coronavirus</kwd><kwd>influenza</kwd><kwd>innate immune system</kwd><kwd>respiratory syncytial virus</kwd><kwd>rhinovirus</kwd><kwd>poly (ICLC)</kwd><kwd>Toll-lik ereceptor 3.</kwd></kwd-group></article-meta></front><floats-group><fig id="F1" position="float"><label>Fig. (1)</label><caption><p>Double-stranded and single-stranded RNA signaling pathway. Double-stranded RNA is recognized in the cytosol by RIG-I or in the
endosome by TLR3, whereas ssRNA is recognized by TLR7 in the endosome. Binding of dsRNA to RIG-I recruits MDA5 and the complex
interacts with IPS-1 present in the mitochondrial membrane. Interaction of IPS-1 with TRAF3, NAK-associated protein 1 (NAP1), IKKε and
TBK1 results in activation of transcription factors (TFs) IRF3 and IRF7 and induction of type I IFN genes. Interaction of IPS-1 with NF-κB
essential modulator (NEMO), receptor-interacting protein 1 (RIP-1) and the IKK complex, or NIK and IKKα results in the release of active
NF-κB and induction of various genes encoding pro-inflammatory cytokines and chemokines. In the endosome, binding of dsRNA with
TLR3 results in the recruitment of TRIF and RIP-1 which can interact with TRAF6 or TRAF3. Interaction with TRAF6 and IL-1 receptorassociated
kinase (IRAK) leads to the induction of pro-inflammatory cytokines through activation of TFs NF-κB and activating protein 1
(AP-1). In the endosome, binding of ssRNA to TLR7 recruits MyD88 which can interact with TRAF6 or TRAF3. The TLR7, MyD88,
TRAF6 pathway intersects with the TLR3 TRAF6 pathway to induce pro-inflammatory cytokines and chemokines. The TLR7, MyD88,
TRAF3 pathway results in activation of TFs IRF5 and IRF7, resulting in induction of type I IFNs [<xref ref-type="bibr" rid="R24">24</xref>, <xref ref-type="bibr" rid="R34">34</xref>]. Apoptosis is also induced
following binding of dsRNA to either TLR3 or RIG-I via FADD/Caspase 8 or TRAF2/Caspase9, respectively [<xref ref-type="bibr" rid="R24">24</xref>]. Influenza virus (IV) NS1
protein can inhibit the signaling pathway by binding to dsRNA preventing its recognition by RIG-I/ TLR3, inhibiting RIG-I, IPS-1, nuclear
translocation of IRF3 or IPS-1-induced apoptosis [<xref ref-type="bibr" rid="R64">64</xref>, <xref ref-type="bibr" rid="R65">65</xref>]. RSV NS2 protein can also inhibit RIG-I, IRF3 and IPS-1-induced apoptosis [<xref ref-type="bibr" rid="R75">75</xref>,
<xref ref-type="bibr" rid="R76">76</xref>]. SARS-Co-V [<xref ref-type="bibr" rid="R83">83</xref>] also inhibits IPS-1-induced apoptosis and rhinovirus (RV) [<xref ref-type="bibr" rid="R88">88</xref>] has been shown to inhibit IPS-1.</p></caption><graphic xlink:href="AIAAMC-10-327_F1"></graphic></fig></floats-group></pmc><affiliations><list></list><tree><noCountry><name sortKey="Christopher, Me" sort="Christopher, Me" uniqKey="Christopher M" first="Me" last="Christopher">Me Christopher</name><name sortKey="Wong, Jp" sort="Wong, Jp" uniqKey="Wong J" first="Jp" last="Wong">Jp Wong</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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