Antibody and inflammatory response‐mediated severity of pandemic 2009 (pH1N1) influenza virus
Identifieur interne : 000E49 ( Istex/Corpus ); précédent : 000E48; suivant : 000E50Antibody and inflammatory response‐mediated severity of pandemic 2009 (pH1N1) influenza virus
Auteurs : Nivedita Tiwari ; Prerna Kapoor ; Tapan N. DholeSource :
- Journal of Medical Virology [ 0146-6615 ] ; 2014-06.
Abstract
Influenza A virus causes significant morbidity and mortality each year worldwide due to antigenic drift, punctuated by infrequent pandemics following antigenic shift. H1N1 subtype of pandemic 2009 (pH1N1) influenza virus lineages has continued to circulate in humans and raised severe concerns about its pandemic developments. The pathogenesis of the disease and its progression as post‐infectious sequelae is not well understood. Moderate inflammatory response protects against the ill effects and hyper‐inflammatory response promotes the pathogenesis in disease progression. Samples were screened by RT‐PCR and classified in pandemic 2009 (pH1N1), Influenza A virus infected patient. Further antibody titer was analyzed by hemagglutination inhibition assay and cytokine/chemokine response by Cytometric bead array assy. Screening of 216 patients shows 63 were belongs to pH1N1 influenza virus infection and 47 were Influenza A virus infected and 106 samples were negative for these viruses, were used as a disease control. Apart from that 100 samples were taken for healthy control. Lower antibody titer was found in patient infected with pH1N1/Influenza A virus and expression of cytokines (IL‐6, IL‐8, and IL‐10) and chemokine MCP‐1 was higher in patient infected with pH1N1 compare to healthy/disease control however there was no significant difference observed in the expression of pro‐inflammatory cytokines TNF‐α and antiviral cytokine IFN‐γ in pH1N1 influenza virus infected patients. J. Med. Virol. 86:1034–1040, 2014. © 2014 Wiley Periodicals, Inc.
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DOI: 10.1002/jmv.23877
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Lower antibody titer was found in patient infected with pH1N1/Influenza A virus and expression of cytokines (IL‐6, IL‐8, and IL‐10) and chemokine MCP‐1 was higher in patient infected with pH1N1 compare to healthy/disease control however there was no significant difference observed in the expression of pro‐inflammatory cytokines TNF‐α and antiviral cytokine IFN‐γ in pH1N1 influenza virus infected patients. J. Med. 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H1N1 subtype of pandemic 2009 (pH1N1) influenza virus lineages has continued to circulate in humans and raised severe concerns about its pandemic developments. The pathogenesis of the disease and its progression as post‐infectious sequelae is not well understood. Moderate inflammatory response protects against the ill effects and hyper‐inflammatory response promotes the pathogenesis in disease progression. Samples were screened by RT‐PCR and classified in pandemic 2009 (pH1N1), Influenza A virus infected patient. Further antibody titer was analyzed by hemagglutination inhibition assay and cytokine/chemokine response by Cytometric bead array assy. Screening of 216 patients shows 63 were belongs to pH1N1 influenza virus infection and 47 were Influenza A virus infected and 106 samples were negative for these viruses, were used as a disease control. Apart from that 100 samples were taken for healthy control. Lower antibody titer was found in patient infected with pH1N1/Influenza A virus and expression of cytokines (IL‐6, IL‐8, and IL‐10) and chemokine MCP‐1 was higher in patient infected with pH1N1 compare to healthy/disease control however there was no significant difference observed in the expression of pro‐inflammatory cytokines TNF‐α and antiviral cytokine IFN‐γ in pH1N1 influenza virus infected patients. <b><i>J. Med. Virol. 86:1034–1040, 2014</i>.</b> © 2014 Wiley Periodicals, Inc.</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="jmv23877-note-0003" numbered="no">The authors declared that they have no conflicts of interest.</note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Antibody and inflammatory response‐mediated severity of pandemic 2009 (pH1N1) influenza virus</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Antibody and Inflammatory Response of pH1N1 Influenza Virus</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Antibody and inflammatory response‐mediated severity of pandemic 2009 (pH1N1) influenza virus</title></titleInfo><name type="personal"><namePart type="given">Nivedita</namePart><namePart type="family">Tiwari</namePart><affiliation>Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, UP, Lucknow, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Prerna</namePart><namePart type="family">Kapoor</namePart><affiliation>Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, UP, Lucknow, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tapan N.</namePart><namePart type="family">Dhole</namePart><affiliation>Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, UP, Lucknow, India</affiliation><affiliation>E-mail: tndhole@sgpgi.ac.in</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2014-06</dateIssued><dateCreated encoding="w3cdtf">2014-02-14</dateCreated><dateCaptured encoding="w3cdtf">2013-10-25</dateCaptured><dateValid encoding="w3cdtf">2013-12-12</dateValid><copyrightDate encoding="w3cdtf">2014</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Influenza A virus causes significant morbidity and mortality each year worldwide due to antigenic drift, punctuated by infrequent pandemics following antigenic shift. H1N1 subtype of pandemic 2009 (pH1N1) influenza virus lineages has continued to circulate in humans and raised severe concerns about its pandemic developments. The pathogenesis of the disease and its progression as post‐infectious sequelae is not well understood. Moderate inflammatory response protects against the ill effects and hyper‐inflammatory response promotes the pathogenesis in disease progression. Samples were screened by RT‐PCR and classified in pandemic 2009 (pH1N1), Influenza A virus infected patient. Further antibody titer was analyzed by hemagglutination inhibition assay and cytokine/chemokine response by Cytometric bead array assy. Screening of 216 patients shows 63 were belongs to pH1N1 influenza virus infection and 47 were Influenza A virus infected and 106 samples were negative for these viruses, were used as a disease control. Apart from that 100 samples were taken for healthy control. Lower antibody titer was found in patient infected with pH1N1/Influenza A virus and expression of cytokines (IL‐6, IL‐8, and IL‐10) and chemokine MCP‐1 was higher in patient infected with pH1N1 compare to healthy/disease control however there was no significant difference observed in the expression of pro‐inflammatory cytokines TNF‐α and antiviral cytokine IFN‐γ in pH1N1 influenza virus infected patients. J. Med. Virol. 86:1034–1040, 2014. © 2014 Wiley Periodicals, Inc.</abstract><note type="funding">National Institute of communicable Diseases, New Delhi</note><note type="funding">Indian Council of Medical Research, Government of India, New Delhi - No. 80/731/2012‐ECD‐I; </note><subject lang="en"><genre>keywords</genre><topic>influenza virus</topic><topic>antibody</topic><topic>cytokines</topic><topic>chemokines and inflammatory response</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Medical Virology</title></titleInfo><titleInfo type="abbreviated"><title>J. 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