In vivo Ebola virus infection leads to a strong innate response in circulating immune cells
Ebola virus is the causative agent of a severe syndrome in humans with a fatality rate that can approach 90 %. During infection, the host immune response is thought to become dysregulated, but the mechanisms through which this happens are not entirely understood. In this study, we analyze RNA sequen...
Gespeichert in:
| Veröffentlicht in: | BMC genomics 2016-09, Vol.17 (1), p.707-707, Article 707 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 707 |
|---|---|
| container_issue | 1 |
| container_start_page | 707 |
| container_title | BMC genomics |
| container_volume | 17 |
| creator | Caballero, Ignacio S Honko, Anna N Gire, Stephen K Winnicki, Sarah M Melé, Marta Gerhardinger, Chiara Lin, Aaron E Rinn, John L Sabeti, Pardis C Hensley, Lisa E Connor, John H |
| description | Ebola virus is the causative agent of a severe syndrome in humans with a fatality rate that can approach 90 %. During infection, the host immune response is thought to become dysregulated, but the mechanisms through which this happens are not entirely understood. In this study, we analyze RNA sequencing data to determine the host response to Ebola virus infection in circulating immune cells.
Approximately half of the 100 genes with the strongest early increases in expression were interferon-stimulated genes, such as ISG15, OAS1, IFIT2, HERC5, MX1 and DHX58. Other highly upregulated genes included cytokines CXCL11, CCL7, IL2RA, IL2R1, IL15RA, and CSF2RB, which have not been previously reported to change during Ebola virus infection. Comparing this response in two different models of exposure (intramuscular and aerosol) revealed a similar signature of infection. The strong innate response in the aerosol model was seen not only in circulating cells, but also in primary and secondary target tissues. Conversely, the innate immune response of vaccinated macaques was almost non-existent. This suggests that the innate response is a major aspect of the cellular response to Ebola virus infection in multiple tissues.
Ebola virus causes a severe infection in humans that is associated with high mortality. The host immune response to virus infection is thought to be an important aspect leading to severe pathology, but the components of this overactive response are not well characterized. Here, we analyzed how circulating immune cells respond to the virus and found that there is a strong innate response dependent on active virus replication. This finding is in stark contrast to in vitro evidence showing a suppression of innate immune signaling, and it suggests that the strong innate response we observe in infected animals may be an important contributor to pathogenesis. |
| doi_str_mv | 10.1186/s12864-016-3060-0 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5011782</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A466570038</galeid><sourcerecordid>A466570038</sourcerecordid><originalsourceid>FETCH-LOGICAL-c528t-272b63a00b7b625b77d1a7a35f6a28e9d6d56dbec5451b3eae2118e1efe9b4a3</originalsourceid><addsrcrecordid>eNptksFu1DAQhi0EoqXwAFyQJS5wSOtxYjt7QaqqAitVQiq9cbAcZ7K4SuzFdlbw9jja0nYr5IPHnm9-e0Y_IW-BnQK08iwBb2VTMZBVzSSr2DNyDI2CioNsnj-Kj8irlG4ZA9Vy8ZIccSVWom2aY_Jj7enO7QK97MJoShjnRJ0f0GYXPB3R9InmQA1NOQa_KTlvMtKIaRt8wnKm1kU7jya7JT1Ns0dqcRzTa_JiMGPCN3f7Cbn5fHlz8bW6-vZlfXF-VVnB21xxxTtZG8Y61UkuOqV6MMrUYpCGt7jqZS9k36EVjYCuRoO8dI-AA666xtQn5NNedjt3E_YWfY5m1NvoJhP_6GCcPsx491Nvwk4LBstAisCHO4EYfs2Ysp5cWjowHsOcNLSghGSciYK-f4Lehjn60l2h-CIIK_ZAbcyIukwzlHftIqrPGymFYqxuC3X6H6qsHidng8fBlfuDgo8HBYXJ-DtvzJySXn-_PmRhz9oYUoo43M8DmF7Mo_fm0cU8ejGPXr797vEg7yv-uaX-C77AvnE</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1825011190</pqid></control><display><type>article</type><title>In vivo Ebola virus infection leads to a strong innate response in circulating immune cells</title><source>SpringerOpen</source><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Springer Journals</source><source>PubMed Central</source><source>EZB Electronic Journals Library</source><source>PubMed Central Open Access</source><creator>Caballero, Ignacio S ; Honko, Anna N ; Gire, Stephen K ; Winnicki, Sarah M ; Melé, Marta ; Gerhardinger, Chiara ; Lin, Aaron E ; Rinn, John L ; Sabeti, Pardis C ; Hensley, Lisa E ; Connor, John H</creator><creatorcontrib>Caballero, Ignacio S ; Honko, Anna N ; Gire, Stephen K ; Winnicki, Sarah M ; Melé, Marta ; Gerhardinger, Chiara ; Lin, Aaron E ; Rinn, John L ; Sabeti, Pardis C ; Hensley, Lisa E ; Connor, John H</creatorcontrib><description>Ebola virus is the causative agent of a severe syndrome in humans with a fatality rate that can approach 90 %. During infection, the host immune response is thought to become dysregulated, but the mechanisms through which this happens are not entirely understood. In this study, we analyze RNA sequencing data to determine the host response to Ebola virus infection in circulating immune cells.
Approximately half of the 100 genes with the strongest early increases in expression were interferon-stimulated genes, such as ISG15, OAS1, IFIT2, HERC5, MX1 and DHX58. Other highly upregulated genes included cytokines CXCL11, CCL7, IL2RA, IL2R1, IL15RA, and CSF2RB, which have not been previously reported to change during Ebola virus infection. Comparing this response in two different models of exposure (intramuscular and aerosol) revealed a similar signature of infection. The strong innate response in the aerosol model was seen not only in circulating cells, but also in primary and secondary target tissues. Conversely, the innate immune response of vaccinated macaques was almost non-existent. This suggests that the innate response is a major aspect of the cellular response to Ebola virus infection in multiple tissues.
Ebola virus causes a severe infection in humans that is associated with high mortality. The host immune response to virus infection is thought to be an important aspect leading to severe pathology, but the components of this overactive response are not well characterized. Here, we analyzed how circulating immune cells respond to the virus and found that there is a strong innate response dependent on active virus replication. This finding is in stark contrast to in vitro evidence showing a suppression of innate immune signaling, and it suggests that the strong innate response we observe in infected animals may be an important contributor to pathogenesis.</description><identifier>ISSN: 1471-2164</identifier><identifier>EISSN: 1471-2164</identifier><identifier>DOI: 10.1186/s12864-016-3060-0</identifier><identifier>PMID: 27595844</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Ebola virus ; Ebolavirus - pathogenicity ; Ebolavirus - physiology ; Gene Expression Profiling - methods ; Gene Expression Regulation ; Gene Regulatory Networks ; Genetic aspects ; Genomics ; Hemorrhagic Fever, Ebola - genetics ; Hemorrhagic Fever, Ebola - immunology ; Hemorrhagic Fever, Ebola - virology ; Immune response ; Immunity, Innate ; Leukocytes, Mononuclear - immunology ; Leukocytes, Mononuclear - metabolism ; Macaca - virology ; Mice ; Physiological aspects ; Sequence Analysis, RNA - methods ; Virus Replication</subject><ispartof>BMC genomics, 2016-09, Vol.17 (1), p.707-707, Article 707</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>The Author(s). 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c528t-272b63a00b7b625b77d1a7a35f6a28e9d6d56dbec5451b3eae2118e1efe9b4a3</citedby><cites>FETCH-LOGICAL-c528t-272b63a00b7b625b77d1a7a35f6a28e9d6d56dbec5451b3eae2118e1efe9b4a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5011782/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5011782/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27915,27916,53782,53784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27595844$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Caballero, Ignacio S</creatorcontrib><creatorcontrib>Honko, Anna N</creatorcontrib><creatorcontrib>Gire, Stephen K</creatorcontrib><creatorcontrib>Winnicki, Sarah M</creatorcontrib><creatorcontrib>Melé, Marta</creatorcontrib><creatorcontrib>Gerhardinger, Chiara</creatorcontrib><creatorcontrib>Lin, Aaron E</creatorcontrib><creatorcontrib>Rinn, John L</creatorcontrib><creatorcontrib>Sabeti, Pardis C</creatorcontrib><creatorcontrib>Hensley, Lisa E</creatorcontrib><creatorcontrib>Connor, John H</creatorcontrib><title>In vivo Ebola virus infection leads to a strong innate response in circulating immune cells</title><title>BMC genomics</title><addtitle>BMC Genomics</addtitle><description>Ebola virus is the causative agent of a severe syndrome in humans with a fatality rate that can approach 90 %. During infection, the host immune response is thought to become dysregulated, but the mechanisms through which this happens are not entirely understood. In this study, we analyze RNA sequencing data to determine the host response to Ebola virus infection in circulating immune cells.
Approximately half of the 100 genes with the strongest early increases in expression were interferon-stimulated genes, such as ISG15, OAS1, IFIT2, HERC5, MX1 and DHX58. Other highly upregulated genes included cytokines CXCL11, CCL7, IL2RA, IL2R1, IL15RA, and CSF2RB, which have not been previously reported to change during Ebola virus infection. Comparing this response in two different models of exposure (intramuscular and aerosol) revealed a similar signature of infection. The strong innate response in the aerosol model was seen not only in circulating cells, but also in primary and secondary target tissues. Conversely, the innate immune response of vaccinated macaques was almost non-existent. This suggests that the innate response is a major aspect of the cellular response to Ebola virus infection in multiple tissues.
Ebola virus causes a severe infection in humans that is associated with high mortality. The host immune response to virus infection is thought to be an important aspect leading to severe pathology, but the components of this overactive response are not well characterized. Here, we analyzed how circulating immune cells respond to the virus and found that there is a strong innate response dependent on active virus replication. This finding is in stark contrast to in vitro evidence showing a suppression of innate immune signaling, and it suggests that the strong innate response we observe in infected animals may be an important contributor to pathogenesis.</description><subject>Animals</subject><subject>Ebola virus</subject><subject>Ebolavirus - pathogenicity</subject><subject>Ebolavirus - physiology</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation</subject><subject>Gene Regulatory Networks</subject><subject>Genetic aspects</subject><subject>Genomics</subject><subject>Hemorrhagic Fever, Ebola - genetics</subject><subject>Hemorrhagic Fever, Ebola - immunology</subject><subject>Hemorrhagic Fever, Ebola - virology</subject><subject>Immune response</subject><subject>Immunity, Innate</subject><subject>Leukocytes, Mononuclear - immunology</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Macaca - virology</subject><subject>Mice</subject><subject>Physiological aspects</subject><subject>Sequence Analysis, RNA - methods</subject><subject>Virus Replication</subject><issn>1471-2164</issn><issn>1471-2164</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptksFu1DAQhi0EoqXwAFyQJS5wSOtxYjt7QaqqAitVQiq9cbAcZ7K4SuzFdlbw9jja0nYr5IPHnm9-e0Y_IW-BnQK08iwBb2VTMZBVzSSr2DNyDI2CioNsnj-Kj8irlG4ZA9Vy8ZIccSVWom2aY_Jj7enO7QK97MJoShjnRJ0f0GYXPB3R9InmQA1NOQa_KTlvMtKIaRt8wnKm1kU7jya7JT1Ns0dqcRzTa_JiMGPCN3f7Cbn5fHlz8bW6-vZlfXF-VVnB21xxxTtZG8Y61UkuOqV6MMrUYpCGt7jqZS9k36EVjYCuRoO8dI-AA666xtQn5NNedjt3E_YWfY5m1NvoJhP_6GCcPsx491Nvwk4LBstAisCHO4EYfs2Ysp5cWjowHsOcNLSghGSciYK-f4Lehjn60l2h-CIIK_ZAbcyIukwzlHftIqrPGymFYqxuC3X6H6qsHidng8fBlfuDgo8HBYXJ-DtvzJySXn-_PmRhz9oYUoo43M8DmF7Mo_fm0cU8ejGPXr797vEg7yv-uaX-C77AvnE</recordid><startdate>20160905</startdate><enddate>20160905</enddate><creator>Caballero, Ignacio S</creator><creator>Honko, Anna N</creator><creator>Gire, Stephen K</creator><creator>Winnicki, Sarah M</creator><creator>Melé, Marta</creator><creator>Gerhardinger, Chiara</creator><creator>Lin, Aaron E</creator><creator>Rinn, John L</creator><creator>Sabeti, Pardis C</creator><creator>Hensley, Lisa E</creator><creator>Connor, John H</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160905</creationdate><title>In vivo Ebola virus infection leads to a strong innate response in circulating immune cells</title><author>Caballero, Ignacio S ; Honko, Anna N ; Gire, Stephen K ; Winnicki, Sarah M ; Melé, Marta ; Gerhardinger, Chiara ; Lin, Aaron E ; Rinn, John L ; Sabeti, Pardis C ; Hensley, Lisa E ; Connor, John H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c528t-272b63a00b7b625b77d1a7a35f6a28e9d6d56dbec5451b3eae2118e1efe9b4a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Ebola virus</topic><topic>Ebolavirus - pathogenicity</topic><topic>Ebolavirus - physiology</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation</topic><topic>Gene Regulatory Networks</topic><topic>Genetic aspects</topic><topic>Genomics</topic><topic>Hemorrhagic Fever, Ebola - genetics</topic><topic>Hemorrhagic Fever, Ebola - immunology</topic><topic>Hemorrhagic Fever, Ebola - virology</topic><topic>Immune response</topic><topic>Immunity, Innate</topic><topic>Leukocytes, Mononuclear - immunology</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Macaca - virology</topic><topic>Mice</topic><topic>Physiological aspects</topic><topic>Sequence Analysis, RNA - methods</topic><topic>Virus Replication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Caballero, Ignacio S</creatorcontrib><creatorcontrib>Honko, Anna N</creatorcontrib><creatorcontrib>Gire, Stephen K</creatorcontrib><creatorcontrib>Winnicki, Sarah M</creatorcontrib><creatorcontrib>Melé, Marta</creatorcontrib><creatorcontrib>Gerhardinger, Chiara</creatorcontrib><creatorcontrib>Lin, Aaron E</creatorcontrib><creatorcontrib>Rinn, John L</creatorcontrib><creatorcontrib>Sabeti, Pardis C</creatorcontrib><creatorcontrib>Hensley, Lisa E</creatorcontrib><creatorcontrib>Connor, John H</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC genomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Caballero, Ignacio S</au><au>Honko, Anna N</au><au>Gire, Stephen K</au><au>Winnicki, Sarah M</au><au>Melé, Marta</au><au>Gerhardinger, Chiara</au><au>Lin, Aaron E</au><au>Rinn, John L</au><au>Sabeti, Pardis C</au><au>Hensley, Lisa E</au><au>Connor, John H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In vivo Ebola virus infection leads to a strong innate response in circulating immune cells</atitle><jtitle>BMC genomics</jtitle><addtitle>BMC Genomics</addtitle><date>2016-09-05</date><risdate>2016</risdate><volume>17</volume><issue>1</issue><spage>707</spage><epage>707</epage><pages>707-707</pages><artnum>707</artnum><issn>1471-2164</issn><eissn>1471-2164</eissn><abstract>Ebola virus is the causative agent of a severe syndrome in humans with a fatality rate that can approach 90 %. During infection, the host immune response is thought to become dysregulated, but the mechanisms through which this happens are not entirely understood. In this study, we analyze RNA sequencing data to determine the host response to Ebola virus infection in circulating immune cells.
Approximately half of the 100 genes with the strongest early increases in expression were interferon-stimulated genes, such as ISG15, OAS1, IFIT2, HERC5, MX1 and DHX58. Other highly upregulated genes included cytokines CXCL11, CCL7, IL2RA, IL2R1, IL15RA, and CSF2RB, which have not been previously reported to change during Ebola virus infection. Comparing this response in two different models of exposure (intramuscular and aerosol) revealed a similar signature of infection. The strong innate response in the aerosol model was seen not only in circulating cells, but also in primary and secondary target tissues. Conversely, the innate immune response of vaccinated macaques was almost non-existent. This suggests that the innate response is a major aspect of the cellular response to Ebola virus infection in multiple tissues.
Ebola virus causes a severe infection in humans that is associated with high mortality. The host immune response to virus infection is thought to be an important aspect leading to severe pathology, but the components of this overactive response are not well characterized. Here, we analyzed how circulating immune cells respond to the virus and found that there is a strong innate response dependent on active virus replication. This finding is in stark contrast to in vitro evidence showing a suppression of innate immune signaling, and it suggests that the strong innate response we observe in infected animals may be an important contributor to pathogenesis.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>27595844</pmid><doi>10.1186/s12864-016-3060-0</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1471-2164 |
| ispartof | BMC genomics, 2016-09, Vol.17 (1), p.707-707, Article 707 |
| issn | 1471-2164 1471-2164 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5011782 |
| source | SpringerOpen; MEDLINE; DOAJ Directory of Open Access Journals; Springer Journals; PubMed Central; EZB Electronic Journals Library; PubMed Central Open Access |
| subjects | Animals Ebola virus Ebolavirus - pathogenicity Ebolavirus - physiology Gene Expression Profiling - methods Gene Expression Regulation Gene Regulatory Networks Genetic aspects Genomics Hemorrhagic Fever, Ebola - genetics Hemorrhagic Fever, Ebola - immunology Hemorrhagic Fever, Ebola - virology Immune response Immunity, Innate Leukocytes, Mononuclear - immunology Leukocytes, Mononuclear - metabolism Macaca - virology Mice Physiological aspects Sequence Analysis, RNA - methods Virus Replication |
| title | In vivo Ebola virus infection leads to a strong innate response in circulating immune cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T19%3A16%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=In%20vivo%20Ebola%20virus%20infection%20leads%20to%20a%20strong%20innate%20response%20in%20circulating%20immune%20cells&rft.jtitle=BMC%20genomics&rft.au=Caballero,%20Ignacio%20S&rft.date=2016-09-05&rft.volume=17&rft.issue=1&rft.spage=707&rft.epage=707&rft.pages=707-707&rft.artnum=707&rft.issn=1471-2164&rft.eissn=1471-2164&rft_id=info:doi/10.1186/s12864-016-3060-0&rft_dat=%3Cgale_pubme%3EA466570038%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1825011190&rft_id=info:pmid/27595844&rft_galeid=A466570038&rfr_iscdi=true |