Transcriptome Signature of Nipah Virus Infected Endothelial Cells

Mathieu, Cyrille; Legras-Lachuer, Catherine; Horvat, Branka

doi:10.5772/21512

Cited by 3 publications

(2 citation statements)

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“…Upregulation of the proteasome and peptide loading complex (PLC) after NiV infection have been described previously. However, selective upregulation of TAP1 and PSMB9 without PSMB8 and PSMB10 in endothelial cells was considered imbalanced [44]. Whereas our findings on type I and II IFN responses (Figure 10) are in line with IFN induction in endothelial cells [45], differences in the level of immunoproteasome and MHC-I upregulation suggest different capacities of endothelial cells and PBEC-ALI cultures to upregulate MHC I antigen presentation after NiV infection.…”

Section: Discussionmentioning

confidence: 47%

Analysis of Nipah Virus Replication and Host Proteome Response Patterns in Differentiated Porcine Airway Epithelial Cells Cultured at the Air–Liquid Interface

Müller

Fischer

Woehnke

et al. 2023

Viruses

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Respiratory tract epithelium infection plays a primary role in Nipah virus (NiV) pathogenesis and transmission. Knowledge about infection dynamics and host responses to NiV infection in respiratory tract epithelia is scarce. Studies in non-differentiated primary respiratory tract cells or cell lines indicate insufficient interferon (IFN) responses. However, studies are lacking in the determination of complex host response patterns in differentiated respiratory tract epithelia for the understanding of NiV replication and spread in swine. Here we characterized infection and spread of NiV in differentiated primary porcine bronchial epithelial cells (PBEC) cultivated at the air–liquid interface (ALI). After the initial infection of only a few apical cells, lateral spread for 12 days with epithelium disruption was observed without releasing substantial amounts of infectious virus from the apical or basal sides. Deep time course proteomics revealed pronounced upregulation of genes related to type I/II IFN, immunoproteasomal subunits, transporter associated with antigen processing (TAP)-mediated peptide transport, and major histocompatibility complex (MHC) I antigen presentation. Spliceosomal factors were downregulated. We propose a model in which NiV replication in PBEC is slowed by a potent and broad type I/II IFN host response with conversion from 26S proteasomes to immunoproteasomal antigen processing and improved MHC I presentation for adaptive immunity priming. NiV induced cytopathic effects could reflect the focal release of cell-associated NiV, which may contribute to efficient airborne viral spread between pigs.

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Section: Discussionmentioning

confidence: 47%

Analysis of Nipah Virus Replication and Host Proteome Response Patterns in Differentiated Porcine Airway Epithelial Cells Cultured at the Air–Liquid Interface

Müller

Fischer

Woehnke

et al. 2023

Viruses

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show abstract

“…Innate immune response plays a critical role in anti-viral host defense and its modulation during NiV infection has been demonstrated in several reports 17, 68– 71 . Robust expression of anti-viral genes in lung tissue, including MX1 , RSAD2 , ISG15 , and OAS1 , during the early stages of NiV infection in ferrets was not sufficient to contain viral dissemination 56 .…”

Section: Nipah Virus Pathogenesis and Animal Modelsmentioning

confidence: 98%

Recent advances in the understanding of Nipah virus immunopathogenesis and anti-viral approaches

2019

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Nipah virus (NiV) is a highly lethal zoonotic paramyxovirus that emerged at the end of last century as a human pathogen capable of causing severe acute respiratory infection and encephalitis. Although NiV provokes serious diseases in numerous mammalian species, the infection seems to be asymptomatic in NiV natural hosts, the fruit bats, which provide a continuous virus source for further outbreaks. Consecutive human-to-human transmission has been frequently observed during outbreaks in Bangladesh and India. NiV was shown to interfere with the innate immune response and interferon type I signaling, restraining the anti-viral response and permitting viral spread. Studies of adaptive immunity in infected patients and animal models have suggested an unbalanced immune response during NiV infection. Here, we summarize some of the recent studies of NiV pathogenesis and NiV-induced modulation of both innate and adaptive immune responses, as well as the development of novel prophylactic and therapeutic approaches, necessary to control this highly lethal emerging infection.

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Analysis of Nipah Virus Replication and Host Proteome Response Patterns in Differentiated Porcine Airway Epithelial Cells Cultured at the Air-Liquid Interface

Müller¹,

Fischer²,

Woehnke³

et al. 2023

Preprint

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Respiratory tract epithelium infection plays a primary role in Nipah virus (NiV) pathogenesis and transmission. Knowledge about infection dynamics and host responses to NiV infection in respir-atory tract epithelia is scarce. Studies in non-differentiated primary respiratory tract cells or cell lines indicate insufficient interferon (IFN) responses. However, studies are lacking to determin-ing complex host response patterns in differentiated respiratory tract epithelia to understand NiV replication and spread in swine. Here we characterized infection and spread of NiV in differenti-ated primary porcine bronchial epithelial cells (PBEC) cultivated at the air-liquid-interface (ALI). After the initial infection of only a few apical cells, lateral spread for 12 days with epithelium disruption was observed without releasing substantial amounts of infectious virus from the api-cal or basal sides. Deep time course proteomics revealed pronounced upregulation of genes re-lated to type I/II- IFN, immunoproteasomal subunits, TAP-mediated peptide transport and MHC I antigen presentation. Spliceosomal factors were downregulated. We propose a model in which NiV replication in PBEC is slowed by a potent and broad type I/II-IFN host response with con-version from 26S proteasomes to immunoproteasomal antigen processing and improved MHC I presentation for adaptive immunity priming. NiV induced cytopathic effects could reflect the focal release of cell-associated NiV, which may contribute to efficient airborne viral spread between pigs.

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Transcriptome Signature of Nipah Virus Infected Endothelial Cells

Cited by 3 publications

References 58 publications

Analysis of Nipah Virus Replication and Host Proteome Response Patterns in Differentiated Porcine Airway Epithelial Cells Cultured at the Air–Liquid Interface

Analysis of Nipah Virus Replication and Host Proteome Response Patterns in Differentiated Porcine Airway Epithelial Cells Cultured at the Air–Liquid Interface

Recent advances in the understanding of Nipah virus immunopathogenesis and anti-viral approaches

Analysis of Nipah Virus Replication and Host Proteome Response Patterns in Differentiated Porcine Airway Epithelial Cells Cultured at the Air-Liquid Interface

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