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Article: MXD1 regulates the H9N2 and H1N1 influenza A virus–induced chemokine expression and their replications in human macrophage

TitleMXD1 regulates the H9N2 and H1N1 influenza A virus–induced chemokine expression and their replications in human macrophage
Authors
Keywordscytokine
influenza virus
MXD1
Issue Date2020
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at https://jlb.onlinelibrary.wiley.com/journal/19383673
Citation
Journal of Leukocyte Biology, 2020, v. 108 n. 5, p. 1631-1640 How to Cite?
AbstractHuman infection with influenza A/Hong Kong/156/97 (H5N1) avian influenza virus is associated with a high mortality rate of 60%. This virus is originated from influenza A/Quail/Hong Kong/G1/97 (H9N2/G1) avian influenza virus. Since the 1990s, four lineages of H9N2 viruses have been circulating in poultry and cause occasional infection in humans in different countries. Due to its zoonotic and genetic reassortment potential, H9N2/G1 and H5N1 viruses are believed to be the next pandemic candidates. Previous reports, including ours, showed that the virulence of avian virus strains correlates with their ability to dysregulate cytokine expression, including TNF‐α, CXCL10, and related chemokines in the virus‐infected cells. However, the transcriptional factors required for this cytokine dysregulation remains undefined. In light of our previous report showing the unconventional role of MYC, an onco‐transcriptional factor, for regulating the antibacterial responses, we hypothesize that the influenza virus–induced cytokine productions may be governed by MYC/MAX/MXD1 network members. Here, we demonstrated that the influenza A/Hong Kong/54/98 (H1N1)‐ or H9N2/G1 virus–induced CXCL10 expressions can be significantly attenuated by knocking down the MXD1 expression in primary human blood macrophages. Indeed, only the MXD1 expression was up‐regulated by both H1N1 and H9N2/G1 viruses, but not other MYC/MAX/MXD1 members. The MXD1 expression and the CXCL10 hyperinduction were dependent on MEK1/2 activation. By using EMSAs, we revealed that MXD1 directly binds to the CXCL10 promoter–derived oligonucleotides upon infection of both viruses. Furthermore, silencing of MXD1 decreased the replication of H9N2 but not H1N1 viruses. Our results provide a new insight into the role of MXD1 for the pathogenicity of avian influenza viruses.
Persistent Identifierhttp://hdl.handle.net/10722/294652
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 1.521
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYim, HCH-
dc.contributor.authorLeon, TYY-
dc.contributor.authorLi, JCB-
dc.date.accessioned2020-12-08T07:40:00Z-
dc.date.available2020-12-08T07:40:00Z-
dc.date.issued2020-
dc.identifier.citationJournal of Leukocyte Biology, 2020, v. 108 n. 5, p. 1631-1640-
dc.identifier.issn0741-5400-
dc.identifier.urihttp://hdl.handle.net/10722/294652-
dc.description.abstractHuman infection with influenza A/Hong Kong/156/97 (H5N1) avian influenza virus is associated with a high mortality rate of 60%. This virus is originated from influenza A/Quail/Hong Kong/G1/97 (H9N2/G1) avian influenza virus. Since the 1990s, four lineages of H9N2 viruses have been circulating in poultry and cause occasional infection in humans in different countries. Due to its zoonotic and genetic reassortment potential, H9N2/G1 and H5N1 viruses are believed to be the next pandemic candidates. Previous reports, including ours, showed that the virulence of avian virus strains correlates with their ability to dysregulate cytokine expression, including TNF‐α, CXCL10, and related chemokines in the virus‐infected cells. However, the transcriptional factors required for this cytokine dysregulation remains undefined. In light of our previous report showing the unconventional role of MYC, an onco‐transcriptional factor, for regulating the antibacterial responses, we hypothesize that the influenza virus–induced cytokine productions may be governed by MYC/MAX/MXD1 network members. Here, we demonstrated that the influenza A/Hong Kong/54/98 (H1N1)‐ or H9N2/G1 virus–induced CXCL10 expressions can be significantly attenuated by knocking down the MXD1 expression in primary human blood macrophages. Indeed, only the MXD1 expression was up‐regulated by both H1N1 and H9N2/G1 viruses, but not other MYC/MAX/MXD1 members. The MXD1 expression and the CXCL10 hyperinduction were dependent on MEK1/2 activation. By using EMSAs, we revealed that MXD1 directly binds to the CXCL10 promoter–derived oligonucleotides upon infection of both viruses. Furthermore, silencing of MXD1 decreased the replication of H9N2 but not H1N1 viruses. Our results provide a new insight into the role of MXD1 for the pathogenicity of avian influenza viruses.-
dc.languageeng-
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at https://jlb.onlinelibrary.wiley.com/journal/19383673-
dc.relation.ispartofJournal of Leukocyte Biology-
dc.rightsSubmitted (preprint) Version This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. Accepted (peer-reviewed) Version This is the peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.-
dc.subjectcytokine-
dc.subjectinfluenza virus-
dc.subjectMXD1-
dc.titleMXD1 regulates the H9N2 and H1N1 influenza A virus–induced chemokine expression and their replications in human macrophage-
dc.typeArticle-
dc.identifier.emailLeon, TYY: tleon@hku.hk-
dc.identifier.emailLi, JCB: jamesli@hku.hk-
dc.identifier.authorityLi, JCB=rp00496-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/JLB.4MA0620-703RR-
dc.identifier.pmid32794336-
dc.identifier.scopuseid_2-s2.0-85089384951-
dc.identifier.hkuros320458-
dc.identifier.volume108-
dc.identifier.issue5-
dc.identifier.spage1631-
dc.identifier.epage1640-
dc.identifier.isiWOS:000568028900001-
dc.publisher.placeUnited Kingdom-

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