guest ::
| Home > Publications Database > Innate immune response to SARS-CoV-2 infection contributes to neuronal damage in human iPSC-derived peripheral neurons. > print |
| Home > Publications Database > Innate immune response to SARS-CoV-2 infection contributes to neuronal damage in human iPSC-derived peripheral neurons. > print |
| 001 | 267514 | ||
| 005 | 20240225002519.0 | ||
| 024 | 7 | _ | |a 10.1002/jmv.29455 |2 doi |
| 024 | 7 | _ | |a pmid:38323709 |2 pmid |
| 024 | 7 | _ | |a 0146-6615 |2 ISSN |
| 024 | 7 | _ | |a 1096-9071 |2 ISSN |
| 024 | 7 | _ | |a altmetric:159198512 |2 altmetric |
| 037 | _ | _ | |a DZNE-2024-00160 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Passos, Vania |b 0 |
| 245 | _ | _ | |a Innate immune response to SARS-CoV-2 infection contributes to neuronal damage in human iPSC-derived peripheral neurons. |
| 260 | _ | _ | |a Bognor Regis [u.a.] |c 2024 |b Wiley |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1708335435_1854 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Severe acute respiratory coronavirus 2 (SARS-CoV-2) causes neurological disease in the peripheral and central nervous system (PNS and CNS, respectively) of some patients. It is not clear whether SARS-CoV-2 infection or the subsequent immune response are the key factors that cause neurological disease. Here, we addressed this question by infecting human induced pluripotent stem cell-derived CNS and PNS neurons with SARS-CoV-2. SARS-CoV-2 infected a low number of CNS neurons and did not elicit a robust innate immune response. On the contrary, SARS-CoV-2 infected a higher number of PNS neurons. This resulted in expression of interferon (IFN) λ1, several IFN-stimulated genes and proinflammatory cytokines. The PNS neurons also displayed alterations characteristic of neuronal damage, as increased levels of sterile alpha and Toll/interleukin receptor motif-containing protein 1, amyloid precursor protein and α-synuclein, and lower levels of cytoskeletal proteins. Interestingly, blockade of the Janus kinase and signal transducer and activator of transcription pathway by Ruxolitinib did not increase SARS-CoV-2 infection, but reduced neuronal damage, suggesting that an exacerbated neuronal innate immune response contributes to pathogenesis in the PNS. Our results provide a basis to study coronavirus disease 2019 (COVID-19) related neuronal pathology and to test future preventive or therapeutic strategies. |
| 536 | _ | _ | |a 352 - Disease Mechanisms (POF4-352) |0 G:(DE-HGF)POF4-352 |c POF4-352 |f POF IV |x 0 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de |
| 650 | _ | 7 | |a JAK/STAT |2 Other |
| 650 | _ | 7 | |a SARM1 |2 Other |
| 650 | _ | 7 | |a SARS-CoV-2 |2 Other |
| 650 | _ | 7 | |a iPSC-derived peripheral neurons |2 Other |
| 650 | _ | 7 | |a interferon |2 Other |
| 650 | _ | 7 | |a neuronal damage |2 Other |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a COVID-19 |2 MeSH |
| 650 | _ | 2 | |a Induced Pluripotent Stem Cells |2 MeSH |
| 650 | _ | 2 | |a SARS-CoV-2 |2 MeSH |
| 650 | _ | 2 | |a Immunity, Innate |2 MeSH |
| 650 | _ | 2 | |a Neurons |2 MeSH |
| 700 | 1 | _ | |a Henkel, Lisa M |b 1 |
| 700 | 1 | _ | |a Wang, Jiayi |b 2 |
| 700 | 1 | _ | |a Zapatero-Belinchón, Francisco J |0 0000-0002-2751-8411 |b 3 |
| 700 | 1 | _ | |a Möller, Rebecca |b 4 |
| 700 | 1 | _ | |a Sun, Guorong |0 0000-0001-7549-7304 |b 5 |
| 700 | 1 | _ | |a Waltl, Inken |0 0000-0001-7518-1035 |b 6 |
| 700 | 1 | _ | |a Schneider, Talia |0 0000-0002-8796-0404 |b 7 |
| 700 | 1 | _ | |a Wachs, Amelie |b 8 |
| 700 | 1 | _ | |a Ritter, Birgit |b 9 |
| 700 | 1 | _ | |a Kropp, Kai A |0 0000-0001-8505-3440 |b 10 |
| 700 | 1 | _ | |a Zhu, Shuyong |b 11 |
| 700 | 1 | _ | |a Deleidi, Michela |0 P:(DE-2719)2810385 |b 12 |
| 700 | 1 | _ | |a Kalinke, Ulrich |0 0000-0003-0503-9564 |b 13 |
| 700 | 1 | _ | |a Schulz, Thomas F |0 0000-0001-8792-5345 |b 14 |
| 700 | 1 | _ | |a Höglinger, Günter |0 P:(DE-2719)2811373 |b 15 |u dzne |
| 700 | 1 | _ | |a Gerold, Gisa |0 0000-0002-1326-5038 |b 16 |
| 700 | 1 | _ | |a Wegner, Florian |b 17 |
| 700 | 1 | _ | |a Viejo-Borbolla, Abel |0 0000-0001-6395-4010 |b 18 |
| 773 | _ | _ | |a 10.1002/jmv.29455 |g Vol. 96, no. 2, p. e29455 |0 PERI:(DE-600)1475090-9 |n 2 |p e29455 |t Journal of medical virology |v 96 |y 2024 |x 0146-6615 |
| 856 | 4 | _ | |u https://pub.dzne.de/record/267514/files/DZNE-2024-00160%20SUP.zip |
| 856 | 4 | _ | |y OpenAccess |u https://pub.dzne.de/record/267514/files/DZNE-2024-00160.pdf |
| 856 | 4 | _ | |y OpenAccess |x pdfa |u https://pub.dzne.de/record/267514/files/DZNE-2024-00160.pdf?subformat=pdfa |
| 909 | C | O | |o oai:pub.dzne.de:267514 |p openaire |p open_access |p VDB |p driver |p dnbdelivery |
| 910 | 1 | _ | |a Deutsches Zentrum für Neurodegenerative Erkrankungen |0 I:(DE-588)1065079516 |k DZNE |b 12 |6 P:(DE-2719)2810385 |
| 910 | 1 | _ | |a External Institute |0 I:(DE-HGF)0 |k Extern |b 15 |6 P:(DE-2719)2811373 |
| 913 | 1 | _ | |a DE-HGF |b Gesundheit |l Neurodegenerative Diseases |1 G:(DE-HGF)POF4-350 |0 G:(DE-HGF)POF4-352 |3 G:(DE-HGF)POF4 |2 G:(DE-HGF)POF4-300 |4 G:(DE-HGF)POF |v Disease Mechanisms |x 0 |
| 914 | 1 | _ | |y 2024 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0200 |2 StatID |b SCOPUS |d 2023-10-21 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0160 |2 StatID |b Essential Science Indicators |d 2023-10-21 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1050 |2 StatID |b BIOSIS Previews |d 2023-10-21 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1190 |2 StatID |b Biological Abstracts |d 2023-10-21 |
| 915 | _ | _ | |a JCR |0 StatID:(DE-HGF)0100 |2 StatID |b J MED VIROL : 2022 |d 2023-10-21 |
| 915 | _ | _ | |a IF >= 10 |0 StatID:(DE-HGF)9910 |2 StatID |b J MED VIROL : 2022 |d 2023-10-21 |
| 915 | _ | _ | |a DEAL Wiley |0 StatID:(DE-HGF)3001 |2 StatID |d 2023-10-21 |w ger |
| 915 | _ | _ | |a WoS |0 StatID:(DE-HGF)0113 |2 StatID |b Science Citation Index Expanded |d 2023-10-21 |
| 915 | _ | _ | |a Creative Commons Attribution-NonCommercial CC BY-NC 4.0 |0 LIC:(DE-HGF)CCBYNC4 |2 HGFVOC |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1030 |2 StatID |b Current Contents - Life Sciences |d 2023-10-21 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0150 |2 StatID |b Web of Science Core Collection |d 2023-10-21 |
| 915 | _ | _ | |a OpenAccess |0 StatID:(DE-HGF)0510 |2 StatID |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0300 |2 StatID |b Medline |d 2023-10-21 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1110 |2 StatID |b Current Contents - Clinical Medicine |d 2023-10-21 |
| 915 | _ | _ | |a Nationallizenz |0 StatID:(DE-HGF)0420 |2 StatID |d 2023-10-21 |w ger |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0199 |2 StatID |b Clarivate Analytics Master Journal List |d 2023-10-21 |
| 920 | 1 | _ | |0 I:(DE-2719)1210011 |k AG Deleidi |l Mitochondria and Inflammation in Neurodegenerative Diseases |x 0 |
| 980 | _ | _ | |a journal |
| 980 | _ | _ | |a VDB |
| 980 | _ | _ | |a UNRESTRICTED |
| 980 | _ | _ | |a I:(DE-2719)1210011 |
| 980 | 1 | _ | |a FullTexts |
| Library | Collection | CLSMajor | CLSMinor | Language | Author |
|---|