Dataset Information

Analysis of Nipah virus replication and host proteome response patterns in differentiated porcine airway epithelial cells cultured at the air-liquid interface

ABSTRACT: Respiratory tract epithelium infection is considered crucial for airborne transmission of Nipah virus (NiV). Knowledge about infection dynamics and host responses to NiV infection in respiratory tract epithelia is scarce. Various studies in non-differentiated primary respiratory tract cells or cell lines indicate limitations in interferon responses. However, comprehensive studies determining complex reaction patterns in differentiated respiratory tract epithelia to understand efficient NiV replication and spread in swine populations are lacking. Here we characterized infection and spread of NiV in differentiated primary porcine bronchial epithelial cells (PBEC) cultivated at the air-liquid-interface (ALI). After initial infection of only a few apical cells, lateral spread for 12 days with disruption of the epithelium 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 interferon (IFN), immunoproteasomal subunits, TAP-mediated peptide transport and MHC I antigen presentation, whereas spliceosomal factors were downregulated. We deduce a model in which NiV replication in pig bronchial epithelia is slowed by a potent and broad type I/II interferon host response with concurrent conversion from 26S proteasomal to immunoproteasomal antigen processing and improved MHC I presentation as a crucial step in adaptive immunity priming. Moreover, strong cytopathic effects observed in infected areas could reflect focal release of cell-associated NiV. Cell-associated NiV may translate into the source of efficient airborne viral spread in vivo with a high local infectious dose leading to high and fast spread of NiV throughout pig herds.

INSTRUMENT(S): timsTOF Pro

ORGANISM(S): Sus Scrofa Domesticus (domestic Pig)

TISSUE(S): Respiratory Epithelial Cell

DISEASE(S): Nipah Virus Encephalitis

SUBMITTER: Axel Karger

LAB HEAD: Axel Karger

PROVIDER: PXD032673 | Pride | 2023-05-10

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	A170.mzTab.gz	Mztab
	A170_2_0d_Slot2-10_1_581.d.zip	Other
	A170_2_0d_Slot2-10_1_581_calibrated.mgf	Mgf
	A170_2_12d_Slot2-16_1_589.d.zip	Other
	A170_2_12d_Slot2-16_1_589_calibrated.mgf	Mgf

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Publications

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

Müller Martin M Fischer Kerstin K Woehnke Elisabeth E Zaeck Luca M LM Prönnecke Christoph C Knittler Michael R MR Karger Axel A Diederich Sandra S Finke Stefan S

Viruses 20230413 4

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 understandi ...[more]

PMID: 37112941

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