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Extracellular Vesicles Released by Enterovirus-Infected EndoC-βH1 Cells Mediate Non-Lytic Viral Spread

Netanyah, Eitan LU orcid ; Calafatti, Matteo LU ; Arvastsson, Jeanette LU ; Cabrera-Rode, Eduardo ; Cilio, Corrado M LU and Sarmiento, Luis LU (2020) In Microorganisms 8(11).
Abstract

While human enteroviruses are generally regarded as a lytic virus, and persistent non-cytolytic enterovirus infection in pancreatic beta cells has been suspected of playing a role in type 1 diabetes pathogenesis. However, it is still unclear how enteroviruses could exit the pancreatic beta cell in a non-lytic manner. This study aimed to investigate the role of beta cell-derived extracellular vesicles (EVs) in the non-lytic enteroviral spread and infection. Size-exclusion chromatography and antibody-based immunoaffinity purification were used to isolate EVs from echovirus 16-infected human beta EndoC-βH1 cells. EVs were then characterized using transmission electron microscopy and Multiplex Bead-Based Flow Cytometry Assay. Virus... (More)

While human enteroviruses are generally regarded as a lytic virus, and persistent non-cytolytic enterovirus infection in pancreatic beta cells has been suspected of playing a role in type 1 diabetes pathogenesis. However, it is still unclear how enteroviruses could exit the pancreatic beta cell in a non-lytic manner. This study aimed to investigate the role of beta cell-derived extracellular vesicles (EVs) in the non-lytic enteroviral spread and infection. Size-exclusion chromatography and antibody-based immunoaffinity purification were used to isolate EVs from echovirus 16-infected human beta EndoC-βH1 cells. EVs were then characterized using transmission electron microscopy and Multiplex Bead-Based Flow Cytometry Assay. Virus production and release were quantified by 50% cell culture infectious dose (CCID50) assay and qRT-PCR. Our results showed that EVs from echovirus 16-infected EndoC-βH1 cells harbor infectious viruses and promote their spread during the pre-lytic phase of infection. Furthermore, the EVs-mediated infection was not inhibited by virus-specific neutralizing antibodies. In summary, this study demonstrated that enteroviruses could exit beta cells non-lytically within infectious EVs, thereby thwarting the access of neutralizing antibodies to viral particles. These data suggest that enterovirus transmission through EVs may contribute to viral dissemination and immune evasion in persistently infected beta cells.

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author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Microorganisms
volume
8
issue
11
article number
1753
publisher
MDPI AG
external identifiers
  • scopus:85096100397
  • pmid:33171580
ISSN
2076-2607
DOI
10.3390/microorganisms8111753
language
English
LU publication?
yes
id
f0a5417d-290f-46ef-b157-854b9cc21f6a
date added to LUP
2020-11-16 08:46:59
date last changed
2024-06-12 23:56:10
@article{f0a5417d-290f-46ef-b157-854b9cc21f6a,
  abstract     = {{<p>While human enteroviruses are generally regarded as a lytic virus, and persistent non-cytolytic enterovirus infection in pancreatic beta cells has been suspected of playing a role in type 1 diabetes pathogenesis. However, it is still unclear how enteroviruses could exit the pancreatic beta cell in a non-lytic manner. This study aimed to investigate the role of beta cell-derived extracellular vesicles (EVs) in the non-lytic enteroviral spread and infection. Size-exclusion chromatography and antibody-based immunoaffinity purification were used to isolate EVs from echovirus 16-infected human beta EndoC-βH1 cells. EVs were then characterized using transmission electron microscopy and Multiplex Bead-Based Flow Cytometry Assay. Virus production and release were quantified by 50% cell culture infectious dose (CCID50) assay and qRT-PCR. Our results showed that EVs from echovirus 16-infected EndoC-βH1 cells harbor infectious viruses and promote their spread during the pre-lytic phase of infection. Furthermore, the EVs-mediated infection was not inhibited by virus-specific neutralizing antibodies. In summary, this study demonstrated that enteroviruses could exit beta cells non-lytically within infectious EVs, thereby thwarting the access of neutralizing antibodies to viral particles. These data suggest that enterovirus transmission through EVs may contribute to viral dissemination and immune evasion in persistently infected beta cells.</p>}},
  author       = {{Netanyah, Eitan and Calafatti, Matteo and Arvastsson, Jeanette and Cabrera-Rode, Eduardo and Cilio, Corrado M and Sarmiento, Luis}},
  issn         = {{2076-2607}},
  language     = {{eng}},
  month        = {{11}},
  number       = {{11}},
  publisher    = {{MDPI AG}},
  series       = {{Microorganisms}},
  title        = {{Extracellular Vesicles Released by Enterovirus-Infected EndoC-βH1 Cells Mediate Non-Lytic Viral Spread}},
  url          = {{http://dx.doi.org/10.3390/microorganisms8111753}},
  doi          = {{10.3390/microorganisms8111753}},
  volume       = {{8}},
  year         = {{2020}},
}