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000267514 037__ $$aDZNE-2024-00160
000267514 041__ $$aEnglish
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000267514 1001_ $$aPassos, Vania$$b0
000267514 245__ $$aInnate immune response to SARS-CoV-2 infection contributes to neuronal damage in human iPSC-derived peripheral neurons.
000267514 260__ $$aBognor Regis [u.a.]$$bWiley$$c2024
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000267514 520__ $$aSevere acute respiratory coronavirus 2 (SARS-CoV-2) causes neurological disease in the peripheral and central nervous system (PNS and CNS, respectively) of some patients. It is not clear whether SARS-CoV-2 infection or the subsequent immune response are the key factors that cause neurological disease. Here, we addressed this question by infecting human induced pluripotent stem cell-derived CNS and PNS neurons with SARS-CoV-2. SARS-CoV-2 infected a low number of CNS neurons and did not elicit a robust innate immune response. On the contrary, SARS-CoV-2 infected a higher number of PNS neurons. This resulted in expression of interferon (IFN) λ1, several IFN-stimulated genes and proinflammatory cytokines. The PNS neurons also displayed alterations characteristic of neuronal damage, as increased levels of sterile alpha and Toll/interleukin receptor motif-containing protein 1, amyloid precursor protein and α-synuclein, and lower levels of cytoskeletal proteins. Interestingly, blockade of the Janus kinase and signal transducer and activator of transcription pathway by Ruxolitinib did not increase SARS-CoV-2 infection, but reduced neuronal damage, suggesting that an exacerbated neuronal innate immune response contributes to pathogenesis in the PNS. Our results provide a basis to study coronavirus disease 2019 (COVID-19) related neuronal pathology and to test future preventive or therapeutic strategies.
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000267514 650_7 $$2Other$$aJAK/STAT
000267514 650_7 $$2Other$$aSARM1
000267514 650_7 $$2Other$$aSARS-CoV-2
000267514 650_7 $$2Other$$aiPSC-derived peripheral neurons
000267514 650_7 $$2Other$$ainterferon
000267514 650_7 $$2Other$$aneuronal damage
000267514 650_2 $$2MeSH$$aHumans
000267514 650_2 $$2MeSH$$aCOVID-19
000267514 650_2 $$2MeSH$$aInduced Pluripotent Stem Cells
000267514 650_2 $$2MeSH$$aSARS-CoV-2
000267514 650_2 $$2MeSH$$aImmunity, Innate
000267514 650_2 $$2MeSH$$aNeurons
000267514 7001_ $$aHenkel, Lisa M$$b1
000267514 7001_ $$aWang, Jiayi$$b2
000267514 7001_ $$00000-0002-2751-8411$$aZapatero-Belinchón, Francisco J$$b3
000267514 7001_ $$aMöller, Rebecca$$b4
000267514 7001_ $$00000-0001-7549-7304$$aSun, Guorong$$b5
000267514 7001_ $$00000-0001-7518-1035$$aWaltl, Inken$$b6
000267514 7001_ $$00000-0002-8796-0404$$aSchneider, Talia$$b7
000267514 7001_ $$aWachs, Amelie$$b8
000267514 7001_ $$aRitter, Birgit$$b9
000267514 7001_ $$00000-0001-8505-3440$$aKropp, Kai A$$b10
000267514 7001_ $$aZhu, Shuyong$$b11
000267514 7001_ $$0P:(DE-2719)2810385$$aDeleidi, Michela$$b12
000267514 7001_ $$00000-0003-0503-9564$$aKalinke, Ulrich$$b13
000267514 7001_ $$00000-0001-8792-5345$$aSchulz, Thomas F$$b14
000267514 7001_ $$0P:(DE-2719)2811373$$aHöglinger, Günter$$b15$$udzne
000267514 7001_ $$00000-0002-1326-5038$$aGerold, Gisa$$b16
000267514 7001_ $$aWegner, Florian$$b17
000267514 7001_ $$00000-0001-6395-4010$$aViejo-Borbolla, Abel$$b18
000267514 773__ $$0PERI:(DE-600)1475090-9$$a10.1002/jmv.29455$$gVol. 96, no. 2, p. e29455$$n2$$pe29455$$tJournal of medical virology$$v96$$x0146-6615$$y2024
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