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IFN-α treatment enhances porcine Arterivirus infection of monocytes via upregulation of the porcine Arterivirus receptor sialoadhesin

Peter Delputte (UGent) , Wander Van Breedam (UGent) , Filip Barbé (UGent) , Kristien Van Reeth (UGent) and Hans Nauwynck (UGent)
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Organization
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.
Keywords
TISSUE MACROPHAGES, INTERFERON, BIOLOGICAL PROPERTIES, MONOCLONAL-ANTIBODIES, IN-VITRO, SIALIC-ACID, ALVEOLAR MACROPHAGES, SHEEP ERYTHROCYTE RECEPTOR, RESPIRATORY SYNDROME VIRUS, ACID-BINDING-RECEPTOR

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MLA
Delputte, Peter, Wander Van Breedam, Filip Barbé, et al. “IFN-α Treatment Enhances Porcine Arterivirus Infection of Monocytes via Upregulation of the Porcine Arterivirus Receptor Sialoadhesin.” JOURNAL OF INTERFERON AND CYTOKINE RESEARCH 27.9 (2007): 757–766. Print.
APA
Delputte, P., Van Breedam, W., Barbé, F., Van Reeth, K., & Nauwynck, H. (2007). IFN-α treatment enhances porcine Arterivirus infection of monocytes via upregulation of the porcine Arterivirus receptor sialoadhesin. JOURNAL OF INTERFERON AND CYTOKINE RESEARCH, 27(9), 757–766.
Chicago author-date
Delputte, Peter, Wander Van Breedam, Filip Barbé, Kristien Van Reeth, and Hans Nauwynck. 2007. “IFN-α Treatment Enhances Porcine Arterivirus Infection of Monocytes via Upregulation of the Porcine Arterivirus Receptor Sialoadhesin.” Journal of Interferon and Cytokine Research 27 (9): 757–766.
Chicago author-date (all authors)
Delputte, Peter, Wander Van Breedam, Filip Barbé, Kristien Van Reeth, and Hans Nauwynck. 2007. “IFN-α Treatment Enhances Porcine Arterivirus Infection of Monocytes via Upregulation of the Porcine Arterivirus Receptor Sialoadhesin.” Journal of Interferon and Cytokine Research 27 (9): 757–766.
Vancouver
1.
Delputte P, Van Breedam W, Barbé F, Van Reeth K, Nauwynck H. IFN-α treatment enhances porcine Arterivirus infection of monocytes via upregulation of the porcine Arterivirus receptor sialoadhesin. JOURNAL OF INTERFERON AND CYTOKINE RESEARCH. 2007;27(9):757–66.
IEEE
[1]
P. Delputte, W. Van Breedam, F. Barbé, K. Van Reeth, and H. Nauwynck, “IFN-α treatment enhances porcine Arterivirus infection of monocytes via upregulation of the porcine Arterivirus receptor sialoadhesin,” JOURNAL OF INTERFERON AND CYTOKINE RESEARCH, vol. 27, no. 9, pp. 757–766, 2007.
@article{383312,
  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.},
  author       = {Delputte, Peter and Van Breedam, Wander and Barbé, Filip and Van Reeth, Kristien and Nauwynck, Hans},
  issn         = {1079-9907},
  journal      = {JOURNAL OF INTERFERON AND CYTOKINE RESEARCH},
  keywords     = {TISSUE MACROPHAGES,INTERFERON,BIOLOGICAL PROPERTIES,MONOCLONAL-ANTIBODIES,IN-VITRO,SIALIC-ACID,ALVEOLAR MACROPHAGES,SHEEP ERYTHROCYTE RECEPTOR,RESPIRATORY SYNDROME VIRUS,ACID-BINDING-RECEPTOR},
  language     = {eng},
  number       = {9},
  pages        = {757--766},
  title        = {IFN-α treatment enhances porcine Arterivirus infection of monocytes via upregulation of the porcine Arterivirus receptor sialoadhesin},
  url          = {http://dx.doi.org/10.1089/jir.2007.0001},
  volume       = {27},
  year         = {2007},
}

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