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Adenoviruses Use Lactoferrin as a Bridge for CAR-Independent Binding to and Infection of Epithelial Cells.

Johansson, Cecilia; Jonsson, Mari; Marttila, Marko; Persson, David; Fan, Xiaolong LU ; Skog, Johan; Frangsmyr, Lars; Wadell, Goran and Arnberg, Niklas (2007) In Journal of Virology 81(2). p.954-963
Abstract
Most adenoviruses bind to the coxsackie- and adenovirus receptor (CAR). Surprisingly, CAR is not expressed apically on polarized cells and is thus not easily available to viruses. Consequently, alternative mechanisms for entry of coxsackievirus and adenovirus into cells have been suggested. We have found that tear fluid promotes adenovirus infection, and we have identified human lactoferrin (HLf) as the tear fluid component responsible for this effect. HLf alone was found to promote binding of adenovirus to epithelial cells in a dose-dependent manner and also infection of epithelial cells by adenovirus. HLf was also found to promote gene delivery from an adenovirus-based vector. The mechanism takes place at the binding stage and functions... (More)
Most adenoviruses bind to the coxsackie- and adenovirus receptor (CAR). Surprisingly, CAR is not expressed apically on polarized cells and is thus not easily available to viruses. Consequently, alternative mechanisms for entry of coxsackievirus and adenovirus into cells have been suggested. We have found that tear fluid promotes adenovirus infection, and we have identified human lactoferrin (HLf) as the tear fluid component responsible for this effect. HLf alone was found to promote binding of adenovirus to epithelial cells in a dose-dependent manner and also infection of epithelial cells by adenovirus. HLf was also found to promote gene delivery from an adenovirus-based vector. The mechanism takes place at the binding stage and functions independently of CAR. Thus, we have identified a novel binding mechanism whereby adenovirus hijacks HLf, a component of the innate immune system, and uses it as a bridge for attachment to host cells. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Virology
volume
81
issue
2
pages
954 - 963
publisher
American Society for Microbiology
external identifiers
  • wos:000243350100051
  • scopus:33846098735
ISSN
1098-5514
DOI
10.1128/JVI.01995-06
language
English
LU publication?
yes
id
907090cc-a4f8-4620-9141-52e105457b02 (old id 163505)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17079302&dopt=Abstract
date added to LUP
2007-07-11 12:07:55
date last changed
2017-03-12 04:07:07
@article{907090cc-a4f8-4620-9141-52e105457b02,
  abstract     = {Most adenoviruses bind to the coxsackie- and adenovirus receptor (CAR). Surprisingly, CAR is not expressed apically on polarized cells and is thus not easily available to viruses. Consequently, alternative mechanisms for entry of coxsackievirus and adenovirus into cells have been suggested. We have found that tear fluid promotes adenovirus infection, and we have identified human lactoferrin (HLf) as the tear fluid component responsible for this effect. HLf alone was found to promote binding of adenovirus to epithelial cells in a dose-dependent manner and also infection of epithelial cells by adenovirus. HLf was also found to promote gene delivery from an adenovirus-based vector. The mechanism takes place at the binding stage and functions independently of CAR. Thus, we have identified a novel binding mechanism whereby adenovirus hijacks HLf, a component of the innate immune system, and uses it as a bridge for attachment to host cells.},
  author       = {Johansson, Cecilia and Jonsson, Mari and Marttila, Marko and Persson, David and Fan, Xiaolong and Skog, Johan and Frangsmyr, Lars and Wadell, Goran and Arnberg, Niklas},
  issn         = {1098-5514},
  language     = {eng},
  number       = {2},
  pages        = {954--963},
  publisher    = {American Society for Microbiology},
  series       = {Journal of Virology},
  title        = {Adenoviruses Use Lactoferrin as a Bridge for CAR-Independent Binding to and Infection of Epithelial Cells.},
  url          = {http://dx.doi.org/10.1128/JVI.01995-06},
  volume       = {81},
  year         = {2007},
}