Title
IFN-<tex>$\alpha$</tex> treatment enhances porcine Arterivirus infection of monocytes via upregulation of the porcine Arterivirus receptor sialoadhesin IFN-<tex>$\alpha$</tex> treatment enhances porcine Arterivirus infection of monocytes via upregulation of the porcine Arterivirus receptor sialoadhesin
Author
Faculty/Department
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences. Pharmacy
Publication type
article
Publication
New York, N.Y. ,
Subject
Chemistry
Biology
Human medicine
Source (journal)
Journal of interferon and cytokine research / International Society for Interferon and Cytokine Research. - New York, N.Y.
Volume/pages
27(2007) :9 , p. 757-766
ISSN
1079-9907
ISI
000249695400003
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Abstract
The Arterivirus porcine reproductive and respiratory syndrome virus ( PRRSV) has a specific tropism for a subset of differentiated macrophages. Porcine sialoadhesin was identified as a PRRSV internalization receptor that is, similarly to sialoadhesins from other species, only expressed on subsets of macrophages. Sialoadhesin is not expressed or only expressed at low levels on monocytes, which might explain why monocytes are largely refractory to PRRSV infection. Different molecules have been identified that regulate human, mouse, or rat sialoadhesin expression in in vitro cultivated monocytes and macrophages, but the effect of these varies greatly between species. In this study, we observed that interferon-alpha ( IFN-alpha) induces sialoadhesin expression on monocytes to levels similar as those on macrophages and that it increases sialoadhesin on macrophages. IFN-alpha-induced sialoadhesin expression was shown to be functional using a red blood cell ( RBC) binding assay. Furthermore, a 2 or 3 day IFN-alpha pretreatment of monocytes caused a 20-fold increase in the numbers of PRRSV-infected monocytes and increased production of infectious virus. We conclude that IFN-alpha, although it is a potent antiviral molecule, upregulated sialoadhesin infection on in vitro cultivated monocytes, which results in enhanced PRRSV infection of monocytes.
E-info
https://repository.uantwerpen.be/docman/iruaauth/ae354a/01f9178.pdf
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