Zika virus infection differentially affects genome-wide transcription in neuronal cells and myeloid dendritic cells
Zika virus (ZIKV) is an emerging mosquito-borne flavivirus that has attracted global attention and international awareness. ZIKV infection exhibits mild symptoms including fever and pains; however, ZIKV has recently been shown to be related to increased birth defects, including microcephaly, in infa...
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| description | Zika virus (ZIKV) is an emerging mosquito-borne flavivirus that has attracted global attention and international awareness. ZIKV infection exhibits mild symptoms including fever and pains; however, ZIKV has recently been shown to be related to increased birth defects, including microcephaly, in infants. In addition, ZIKV is related to the onset of neurological disorders, such as a type of paralysis similar to Guillain-Barré syndrome. However, the mechanisms through which ZIKV affect neuronal cells and myeloid dendritic cells and how ZIKV avoids host immunity are unclear. Accordingly, in this study, we analyzed RNA sequencing data from ZIKV-infected neuronal cells and myeloid dendritic cells by comparative network analyses using protein-protein interaction information. Comparative network analysis revealed major genes showing differential changes in the peripheral neurons, neural crest cells, and myeloid dendritic cells after ZIKV infection. The genes were related to DNA repair systems and prolactin signaling as well as the interferon signaling, neuroinflammation, and cell cycle pathways. These pathways were interconnected by the interaction of proteins in the pathway and significantly regulated by ZIKV infection in neuronal cells and myeloid dendritic cells. Our analysis showed that neuronal cell damage occurred through up-regulation of neuroinflammation and down-regulation of the DNA repair system, but not in myeloid dendritic cells. Interestingly, immune escape by ZIKV infection could be caused by downregulation of prolactin signaling including IRS2, PIK3C3, JAK3, STAT3, and IRF1 as well as mitochondria dysfunction and oxidative phosphorylation in myeloid dendritic cells. These findings provide insight into the mechanisms of ZIKV infection in the host and the association of ZIKV with neurological and immunological symptoms, which may facilitate the development of therapeutic agents and vaccines. |
| doi_str_mv | 10.1371/journal.pone.0231049 |
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ZIKV infection exhibits mild symptoms including fever and pains; however, ZIKV has recently been shown to be related to increased birth defects, including microcephaly, in infants. In addition, ZIKV is related to the onset of neurological disorders, such as a type of paralysis similar to Guillain-Barré syndrome. However, the mechanisms through which ZIKV affect neuronal cells and myeloid dendritic cells and how ZIKV avoids host immunity are unclear. Accordingly, in this study, we analyzed RNA sequencing data from ZIKV-infected neuronal cells and myeloid dendritic cells by comparative network analyses using protein-protein interaction information. Comparative network analysis revealed major genes showing differential changes in the peripheral neurons, neural crest cells, and myeloid dendritic cells after ZIKV infection. The genes were related to DNA repair systems and prolactin signaling as well as the interferon signaling, neuroinflammation, and cell cycle pathways. These pathways were interconnected by the interaction of proteins in the pathway and significantly regulated by ZIKV infection in neuronal cells and myeloid dendritic cells. Our analysis showed that neuronal cell damage occurred through up-regulation of neuroinflammation and down-regulation of the DNA repair system, but not in myeloid dendritic cells. Interestingly, immune escape by ZIKV infection could be caused by downregulation of prolactin signaling including IRS2, PIK3C3, JAK3, STAT3, and IRF1 as well as mitochondria dysfunction and oxidative phosphorylation in myeloid dendritic cells. These findings provide insight into the mechanisms of ZIKV infection in the host and the association of ZIKV with neurological and immunological symptoms, which may facilitate the development of therapeutic agents and vaccines.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0231049</identifier><identifier>PMID: 32287277</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Apoptosis ; Archives & records ; Biology and Life Sciences ; Birth defects ; Cell cycle ; Chemical compounds ; Congenital defects ; Dendritic cells ; Dendritic structure ; Deoxyribonucleic acid ; DNA ; DNA repair ; Down-regulation ; Fever ; Gene expression ; Gene sequencing ; Genes ; Genomes ; Guillain-Barre syndrome ; Immunology ; Infants ; Infections ; Inflammation ; Interferon ; Interferon regulatory factor 1 ; Medicine and Health Sciences ; Microcephaly ; Microencephaly ; Mitochondria ; Mosquitoes ; Network analysis ; Neural crest ; Neurological diseases ; Oxidative phosphorylation ; Paralysis ; Pathogenesis ; Pharmacology ; Phosphorylation ; Prolactin ; Protein interaction ; Proteins ; R&D ; Repair ; Research & development ; Ribonucleic acid ; RNA ; Signal transduction ; Signaling ; Signs and symptoms ; Stat3 protein ; Stem cells ; Toxicology ; Transcription ; Vaccines ; Vector-borne diseases ; Viruses ; West Nile virus ; Zika virus</subject><ispartof>PloS one, 2020-04, Vol.15 (4), p.e0231049</ispartof><rights>2020 Park et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 Park et al 2020 Park et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-5a1d7f529e57a0f0dae3ec3615c3a90b64b7278d2ed5e6678d5b5f53e250657d3</citedby><cites>FETCH-LOGICAL-c526t-5a1d7f529e57a0f0dae3ec3615c3a90b64b7278d2ed5e6678d5b5f53e250657d3</cites><orcidid>0000-0002-9452-5849</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156053/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156053/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32287277$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Park, Tamina</creatorcontrib><creatorcontrib>Kang, Myung-Gyun</creatorcontrib><creatorcontrib>Baek, Seung-Hwa</creatorcontrib><creatorcontrib>Lee, Chang Hoon</creatorcontrib><creatorcontrib>Park, Daeui</creatorcontrib><title>Zika virus infection differentially affects genome-wide transcription in neuronal cells and myeloid dendritic cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Zika virus (ZIKV) is an emerging mosquito-borne flavivirus that has attracted global attention and international awareness. ZIKV infection exhibits mild symptoms including fever and pains; however, ZIKV has recently been shown to be related to increased birth defects, including microcephaly, in infants. In addition, ZIKV is related to the onset of neurological disorders, such as a type of paralysis similar to Guillain-Barré syndrome. However, the mechanisms through which ZIKV affect neuronal cells and myeloid dendritic cells and how ZIKV avoids host immunity are unclear. Accordingly, in this study, we analyzed RNA sequencing data from ZIKV-infected neuronal cells and myeloid dendritic cells by comparative network analyses using protein-protein interaction information. Comparative network analysis revealed major genes showing differential changes in the peripheral neurons, neural crest cells, and myeloid dendritic cells after ZIKV infection. The genes were related to DNA repair systems and prolactin signaling as well as the interferon signaling, neuroinflammation, and cell cycle pathways. These pathways were interconnected by the interaction of proteins in the pathway and significantly regulated by ZIKV infection in neuronal cells and myeloid dendritic cells. Our analysis showed that neuronal cell damage occurred through up-regulation of neuroinflammation and down-regulation of the DNA repair system, but not in myeloid dendritic cells. Interestingly, immune escape by ZIKV infection could be caused by downregulation of prolactin signaling including IRS2, PIK3C3, JAK3, STAT3, and IRF1 as well as mitochondria dysfunction and oxidative phosphorylation in myeloid dendritic cells. These findings provide insight into the mechanisms of ZIKV infection in the host and the association of ZIKV with neurological and immunological symptoms, which may facilitate the development of therapeutic agents and vaccines.</description><subject>Apoptosis</subject><subject>Archives & records</subject><subject>Biology and Life Sciences</subject><subject>Birth defects</subject><subject>Cell cycle</subject><subject>Chemical compounds</subject><subject>Congenital defects</subject><subject>Dendritic cells</subject><subject>Dendritic structure</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA repair</subject><subject>Down-regulation</subject><subject>Fever</subject><subject>Gene expression</subject><subject>Gene sequencing</subject><subject>Genes</subject><subject>Genomes</subject><subject>Guillain-Barre syndrome</subject><subject>Immunology</subject><subject>Infants</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Interferon</subject><subject>Interferon regulatory factor 1</subject><subject>Medicine and Health Sciences</subject><subject>Microcephaly</subject><subject>Microencephaly</subject><subject>Mitochondria</subject><subject>Mosquitoes</subject><subject>Network analysis</subject><subject>Neural crest</subject><subject>Neurological diseases</subject><subject>Oxidative phosphorylation</subject><subject>Paralysis</subject><subject>Pathogenesis</subject><subject>Pharmacology</subject><subject>Phosphorylation</subject><subject>Prolactin</subject><subject>Protein interaction</subject><subject>Proteins</subject><subject>R&D</subject><subject>Repair</subject><subject>Research & development</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Signs and symptoms</subject><subject>Stat3 protein</subject><subject>Stem cells</subject><subject>Toxicology</subject><subject>Transcription</subject><subject>Vaccines</subject><subject>Vector-borne diseases</subject><subject>Viruses</subject><subject>West Nile virus</subject><subject>Zika 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virus infection differentially affects genome-wide transcription in neuronal cells and myeloid dendritic cells</title><author>Park, Tamina ; Kang, Myung-Gyun ; Baek, Seung-Hwa ; Lee, Chang Hoon ; Park, Daeui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-5a1d7f529e57a0f0dae3ec3615c3a90b64b7278d2ed5e6678d5b5f53e250657d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Apoptosis</topic><topic>Archives & records</topic><topic>Biology and Life Sciences</topic><topic>Birth defects</topic><topic>Cell cycle</topic><topic>Chemical compounds</topic><topic>Congenital defects</topic><topic>Dendritic cells</topic><topic>Dendritic structure</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA repair</topic><topic>Down-regulation</topic><topic>Fever</topic><topic>Gene expression</topic><topic>Gene sequencing</topic><topic>Genes</topic><topic>Genomes</topic><topic>Guillain-Barre syndrome</topic><topic>Immunology</topic><topic>Infants</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Interferon</topic><topic>Interferon regulatory factor 1</topic><topic>Medicine and Health Sciences</topic><topic>Microcephaly</topic><topic>Microencephaly</topic><topic>Mitochondria</topic><topic>Mosquitoes</topic><topic>Network analysis</topic><topic>Neural crest</topic><topic>Neurological diseases</topic><topic>Oxidative phosphorylation</topic><topic>Paralysis</topic><topic>Pathogenesis</topic><topic>Pharmacology</topic><topic>Phosphorylation</topic><topic>Prolactin</topic><topic>Protein interaction</topic><topic>Proteins</topic><topic>R&D</topic><topic>Repair</topic><topic>Research & development</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Signs and symptoms</topic><topic>Stat3 protein</topic><topic>Stem 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Park, Tamina</au><au>Kang, Myung-Gyun</au><au>Baek, Seung-Hwa</au><au>Lee, Chang Hoon</au><au>Park, Daeui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Zika virus infection differentially affects genome-wide transcription in neuronal cells and myeloid dendritic cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2020-04-14</date><risdate>2020</risdate><volume>15</volume><issue>4</issue><spage>e0231049</spage><pages>e0231049-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Zika virus (ZIKV) is an emerging mosquito-borne flavivirus that has attracted global attention and international awareness. ZIKV infection exhibits mild symptoms including fever and pains; however, ZIKV has recently been shown to be related to increased birth defects, including microcephaly, in infants. In addition, ZIKV is related to the onset of neurological disorders, such as a type of paralysis similar to Guillain-Barré syndrome. However, the mechanisms through which ZIKV affect neuronal cells and myeloid dendritic cells and how ZIKV avoids host immunity are unclear. Accordingly, in this study, we analyzed RNA sequencing data from ZIKV-infected neuronal cells and myeloid dendritic cells by comparative network analyses using protein-protein interaction information. Comparative network analysis revealed major genes showing differential changes in the peripheral neurons, neural crest cells, and myeloid dendritic cells after ZIKV infection. The genes were related to DNA repair systems and prolactin signaling as well as the interferon signaling, neuroinflammation, and cell cycle pathways. These pathways were interconnected by the interaction of proteins in the pathway and significantly regulated by ZIKV infection in neuronal cells and myeloid dendritic cells. Our analysis showed that neuronal cell damage occurred through up-regulation of neuroinflammation and down-regulation of the DNA repair system, but not in myeloid dendritic cells. Interestingly, immune escape by ZIKV infection could be caused by downregulation of prolactin signaling including IRS2, PIK3C3, JAK3, STAT3, and IRF1 as well as mitochondria dysfunction and oxidative phosphorylation in myeloid dendritic cells. These findings provide insight into the mechanisms of ZIKV infection in the host and the association of ZIKV with neurological and immunological symptoms, which may facilitate the development of therapeutic agents and vaccines.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>32287277</pmid><doi>10.1371/journal.pone.0231049</doi><orcidid>https://orcid.org/0000-0002-9452-5849</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Public Library of Science (PLoS) Journals Open Access; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Apoptosis Archives & records Biology and Life Sciences Birth defects Cell cycle Chemical compounds Congenital defects Dendritic cells Dendritic structure Deoxyribonucleic acid DNA DNA repair Down-regulation Fever Gene expression Gene sequencing Genes Genomes Guillain-Barre syndrome Immunology Infants Infections Inflammation Interferon Interferon regulatory factor 1 Medicine and Health Sciences Microcephaly Microencephaly Mitochondria Mosquitoes Network analysis Neural crest Neurological diseases Oxidative phosphorylation Paralysis Pathogenesis Pharmacology Phosphorylation Prolactin Protein interaction Proteins R&D Repair Research & development Ribonucleic acid RNA Signal transduction Signaling Signs and symptoms Stat3 protein Stem cells Toxicology Transcription Vaccines Vector-borne diseases Viruses West Nile virus Zika virus |
| title | Zika virus infection differentially affects genome-wide transcription in neuronal cells and myeloid dendritic cells |
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