Advanced search
1 file | 218.46 KB

The intriguing game of porcine reproductive and respiratory syndrome virus with different macrophage subsets determines the virological and clinical outcome

Hans Nauwynck (UGent) , Ilias Frydas (UGent) , Ivan Trus (UGent) , Isaura Christiaens (UGent) , Caroline Bonckaert (UGent) and Wander Van Breedam (UGent)
Author
Organization
Abstract
A new disease, characterized by reproductive disorders and respiratory problems emerged in the late eighties in Western Europe and Northern America. It was caused by an arterivirus. Based on the clinical picture, it was called porcine reproductive and respiratory syndrome virus (PRRSV). By serological and genetic analysis, it became clear that on the two continents two different types were circulating, a European type (euPRRSV) and an American type (amPRRSV) and that the virus circulated already for a longer time in Eastern Europe and Northern America. This is very indicative for an increase of pathogenicity of PRRSV during that period. Later, the pathogenicity further increased. In the US, atypical strains were identified in the mid nineties. In 2006, the genetic clock created killer strains in the two types at two totally different locations: high fever disease strains in Asia and subtype 2 and 3 strains in Eastern Europe. Based on these data, it is clear that the virus is in full evolution. The target cell of PRRSV is the macrophage, a central Player In both innate and adaptive immunity. The increase in pathogenicity in time can be explained by a different behavior of the infected cell (cytokine pattern) and the type & number of-different subsets that are infected. Macrophages consist of several subsets with different functions and dependent of the type and number that are infected with PRRSV different virological and clinical outcomes can be obtained. The first isolated euPRRSV, Lelystad virus (LV), starts its replication in nasopharyngeal lymphoid tissues and lung macrophages, followed by a low level viremia and is finally replicating in all lymphoid organs and placenta. The molecular interplay between LV-like viruses and macrophage has been fully elucidated. It starts with the interaction of sialic acids on the GP5/M complex interacting with sialoadhesin, leading to the uptake of the virus. Upon a pH drop and protease activation, the virus disassembles and the genome is released, resulting in replication and transcription. This disassembly is coordinated by the interaction of the GP2/GP3/GP4 complex with CD163. CD163 is a molecule that is present in all monocytes/macrophages. Therefore, once PRRSV enters a macrophage, it infects. The first isolated amPRRSV, VR2332, is replicating in more subsets of macrophages than LV. In the upper respiratory tract, it also infects nasal macrophages, which form a very important first line of defense in the upper respiratory tract. These macrophages do not possess sialoadhesin and therefore, it uses an additional internalization receptor. The possibility of this virus to grow in more subsets in the respiratory tract explains its strong power to spread via airborne route, to cause respiratory problems and to induce a high level viremia. The subtype 2/3 euPRRSV and high fever amPRRSV are also replicating in a broad range of sialoadhesin positive macrophages in lungs. lymphoid tissues and placenta and sialoadhesin negative macrophages in the upper respiratory tract (nasal macrophages). It is believed that these strains are using even more subsets of macrophages than LV and VR2332, explaining the extremely high replication and severe clinical problems. It looks like PRRSV is finding a very efficient way to increase its replication power in macrophages. More work should be done on the identification of the range of receptors that are involved in the macrophage tropism of PRRSV strains in order to explain this evolution. Because PRRSV can use the human homologs of sialoadhesin and CD163 to infect cells, one should be aware of the danger that this virus may pose to man.

Downloads

  • (...).pdf
    • full text
    • |
    • UGent only
    • |
    • PDF
    • |
    • 218.46 KB

Citation

Please use this url to cite or link to this publication:

Chicago
Nauwynck, Hans, Ilias Frydas, Ivan Trus, Isaura Christiaens, Caroline Bonckaert, and Wander Van Breedam. 2014. “The Intriguing Game of Porcine Reproductive and Respiratory Syndrome Virus with Different Macrophage Subsets Determines the Virological and Clinical Outcome.” In XIIIth International Nidovirus Symposium : Abstracts, 43–44.
APA
Nauwynck, H., Frydas, I., Trus, I., Christiaens, I., Bonckaert, C., & Van Breedam, W. (2014). The intriguing game of porcine reproductive and respiratory syndrome virus with different macrophage subsets determines the virological and clinical outcome. XIIIth International Nidovirus Symposium : abstracts (pp. 43–44). Presented at the 13th International Nidovirus Symposium.
Vancouver
1.
Nauwynck H, Frydas I, Trus I, Christiaens I, Bonckaert C, Van Breedam W. The intriguing game of porcine reproductive and respiratory syndrome virus with different macrophage subsets determines the virological and clinical outcome. XIIIth International Nidovirus Symposium : abstracts. 2014. p. 43–4.
MLA
Nauwynck, Hans, Ilias Frydas, Ivan Trus, et al. “The Intriguing Game of Porcine Reproductive and Respiratory Syndrome Virus with Different Macrophage Subsets Determines the Virological and Clinical Outcome.” XIIIth International Nidovirus Symposium : Abstracts. 2014. 43–44. Print.
@inproceedings{5984277,
  abstract     = {A new disease, characterized by reproductive disorders and respiratory problems emerged in the late eighties in Western Europe and Northern America. It was caused by an arterivirus. Based on the clinical picture, it was called porcine reproductive and respiratory syndrome virus (PRRSV). By serological and genetic analysis, it became clear that on the two continents two different types were circulating, a European type (euPRRSV) and an American type (amPRRSV) and that the virus circulated already for a longer time in Eastern Europe and Northern America. This is very indicative for an increase of pathogenicity of PRRSV during that period. Later, the pathogenicity further increased. In the US, atypical strains were identified in the mid nineties. In 2006, the genetic clock created killer strains in the two types at two totally different locations: high fever disease strains in Asia and subtype 2 and 3 strains in Eastern Europe. Based on these data, it is clear that the virus is in full evolution.
The target cell of PRRSV is the macrophage, a central Player In both innate and adaptive immunity. The increase in pathogenicity in time can be explained by a different behavior of the infected cell (cytokine pattern) and the type \& number of-different subsets that are infected. Macrophages consist of several subsets with different functions and dependent of the type and number that are infected with PRRSV different virological and clinical outcomes can be obtained. The first isolated euPRRSV, Lelystad virus (LV), starts its replication in nasopharyngeal lymphoid tissues and lung macrophages, followed by a low level viremia and is finally replicating in all lymphoid organs and placenta. The molecular interplay between LV-like viruses and macrophage has been fully elucidated. It starts with the interaction of sialic acids on the GP5/M complex interacting with sialoadhesin, leading to the uptake of the virus. Upon a pH drop and protease activation, the virus disassembles and the genome is released, resulting in replication and transcription. This disassembly is coordinated by the interaction of the GP2/GP3/GP4 complex with CD163. CD163 is a molecule that is present in all monocytes/macrophages. Therefore, once PRRSV enters a macrophage, it infects. The first isolated amPRRSV, VR2332, is replicating in more subsets of macrophages than LV. In the upper respiratory tract, it also infects nasal macrophages, which form a very important first line of defense in the upper respiratory tract. These macrophages do not possess sialoadhesin and therefore, it uses an additional internalization receptor. The possibility of this virus to grow in more subsets in the respiratory tract explains its strong power to spread via airborne route, to cause respiratory problems and to induce a high level viremia. The subtype 2/3 euPRRSV and high fever amPRRSV are also replicating in a broad range of sialoadhesin positive macrophages in lungs. lymphoid tissues and placenta and sialoadhesin negative macrophages in the upper respiratory tract (nasal macrophages). It is believed that these strains are using even more subsets of macrophages than LV and VR2332, explaining the extremely high replication and severe clinical problems.
It looks like PRRSV is finding a very efficient way to increase its replication power in macrophages. More work should be done on the identification of the range of receptors that are involved in the macrophage tropism of PRRSV strains in order to explain this evolution. Because PRRSV can use the human homologs of sialoadhesin and CD163 to infect cells, one should be aware of the danger that this virus may pose to man.},
  articleno    = {abstract SI.SP-06},
  author       = {Nauwynck, Hans and Frydas, Ilias and Trus, Ivan and Christiaens, Isaura and Bonckaert, Caroline and Van Breedam, Wander},
  booktitle    = {XIIIth International Nidovirus Symposium : abstracts},
  language     = {eng},
  location     = {Salamanca, Spain},
  pages        = {abstract SI.SP-06:43--abstract SI.SP-06:44},
  title        = {The intriguing game of porcine reproductive and respiratory syndrome virus with different macrophage subsets determines the virological and clinical outcome},
  year         = {2014},
}