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Recent example of PRRSV Type 1 virus-host evolution involving nasal macrophages
As explained in our previous article, the PRRSV Type 1 has been evolving and there was clear evidence of this fact in 2013 with the characterization of a new strain discovered in nursery animals in Belgium that was named ‘Flanders 13’. Swine vets in the field described the clinical signs of this strain as an ‘endemic influenza’. His research demonstrated that the virus had evolved. It was not only able to infect alveolar macrophages; it could also now infect nasal macrophages at high levels (Lelystad virus (LV) has a low tropism for these cells). This replication in nasal macrophages was already happening with the PRRSV Type 2 from the very beginning (North American PRRSV Type 2 VR-2332 strain).
In the nose, this new population of impacted macrophages were sialoadhesine negative. He described them as ‘superficial nasal macrophages’ because they are only found in the lamina propria of the nasal mucosa. This evolution of the virus-host interaction triggered the virus’ ability to spread in between pigs (‘survival of the fittest’ principle). Because the transmission of PRRSV Type 1 was not very effective in Europe in the nineties (it took one whole finishing period for LV-like viruses to infect all present pigs) which was in strong contrast with the circulating PRRSV Type 2 strains in the US, he and most other EU researchers had previously criticized the North American focus on the ability of PRRSV to be transmitted in aerosols. With the new insights in the new targets, he fully understands the differences in transmission behavior of the two PRRSV types in the nineties.
What can we expect from future PRRSV Type 1 virus-host evolution based on Nauwynck’s research?
Nauwynck’s research indicates that the virus is likely to evolve towards a syndrome characterized by the presence of high fever and increased blood vessel permeability. He has identified the presence of sialoadhesine negative macrophages in veins which may become infected by PRRSV. He is convinced that getting a tropism for this population of macrophages likely explains the evolution and emergence of highly pathogenic PRRSV strains in Belarus (Lena strain) and China (high fever strains), and that the same phenomenon explains what is currently happening in the United States. He describes the evolution of the virus as a ticking time bomb and that it is only a matter of time before other PRRSV lineages move through the same different evolutionary stages (alveolar macrophages, nasal macrophages, venous macrophages) in their respective parts of the world (Image 1).
The European strain is still 10 years behind in evolution when compared to other parts of the world.
What is the reason of this evolutionary delay in EU? In 1990, Dr Nauwynck was an active member of a group of researchers studying the first PRRS outbreaks in Germany. He believes that the original source of the virus was circulating in the wild in Russia or China for a long period of time. In 1990, after the fall of the Iron Curtain, Germany became infected with a low virulent strain which later on spread over The Netherlands and Belgium and the rest of Western Europe. This was the strain that was isolated by the Lelystad group in 1991. In contrast, North America was infected with different viral clusters that were genetically distinct from each other. These viral clusters were simultaneously circulating which resulted in increased diversity and rapid evolution of the virus. The same happened in eastern parts of Europe, Russia and China.
Lelystad-like viruses that were detected for the first time in Germany, The Netherlands and Belgium, formed a very small cluster of PRRSV strains that went all over the Western European territory, creating a population of closely-related viruses with a lower virulence compared to the other viruses that were circulating at that moment. Dr Nauwynck is convinced that the Western European PRRSV strains are about 10 years behind in their virus-macrophage evolution compared to strains from Russia, China, and North American.
Within the EU, Italy always seems to be the leader in evolutionary changes of PRRSV. He is not sure how to explain this observation. One theory may be that the extended finishing period of pigs for the production of Parma ham, provides a better environment for the virus to evolve faster in individual pigs and pig populations. In the early 2000’s, his group was able to demonstrate that Italian pigs were no longer fully protected against the circulating Italian PRRSV strains with the standard vaccine. This phenomenon is evident again in Italy with present strains that may cause high fever for several weeks. He believes that these observations are indicators of what is likely to happen in the future across Western Europe.
