Unmasking the PRRSV Puzzle: New Recombinant Strains Emerge in China
Hey there! Let’s chat about something pretty important happening in the world of pig farming – specifically, a tricky virus called Porcine Reproductive and Respiratory Syndrome Virus, or PRRSV for short. If you’re involved in the swine industry, you know this virus is a major headache, causing huge economic losses globally. It’s like a constantly shifting target, and lately, things have gotten even more complicated in China.
See, PRRSV comes in different types, and the one we’re talking about here is PRRSV-2, which is the dominant type in China. Now, this virus is already known for evolving, but what’s been happening recently is particularly interesting, and frankly, a bit worrying. We’re seeing a lot of *recombination* – that’s when different strains of the virus swap genetic material, creating entirely new versions. Think of it like mixing and matching different pieces from various puzzles to make a brand new, potentially more challenging puzzle.
In China, there are several main “lineages” or families of PRRSV-2 circulating: Lineage 1 (like the NADC30 strain), Lineage 3 (QYYZ-like), Lineage 5 (VR2332-like), and Lineage 8 (JXA1-like, which includes the notorious highly pathogenic HP-PRRSV). For a while now, NADC30-like strains have been getting cozy with these local Chinese strains, leading to some complex new recombinant viruses.
Recently, researchers spotted two new recombinant PRRSV-2 strains in Fujian province, China, back in 2017 and 2018. What makes these two stand out is that they seem to be recombinants from *four* different lineages (1, 3, 5, and 8)! That’s quite the genetic cocktail. But here’s the thing: we didn’t know much about how nasty these new isolates actually were.
So, this study I’m looking at dives deep into these two strains, named FJLIUY-2017 and PRRSV2/CN/G8/2018. The goal was to figure out their genetic makeup and, crucially, test their pathogenicity – basically, how sick they make piglets.
Getting to Know the Viruses
First off, the scientists had to isolate these viruses. They used special cells, like porcine alveolar macrophages (PAMs) and MARC-145CD163 cells, which are like the virus’s preferred hangouts in the lab. Once they had the viruses isolated, they got down to the nitty-gritty of their genetics.
They sequenced the complete genomes of both FJLIUY-2017 and PRRSV2/CN/G8/2018. This is like reading the virus’s entire instruction manual. What they found was pretty telling: the two strains shared about 89.2% identity with each other, which isn’t super high. Even more interesting, they had low similarity (less than 92%) to the PRRSV sequences already out there in public databases. This hinted that they were indeed something new.
Using fancy software, they built phylogenetic trees (like a family tree for viruses) and looked for signs of recombination. And bingo! The analysis strongly suggested that both strains were recombinant viruses, pulling genetic pieces from lineages 1, 3, 5.1, and 8.7.
For example, PRRSV2/CN/G8/2018 seemed to have its main backbone from a Lineage 1 (NADC30-like) virus, but it had bits from Lineage 8.7 (JXA1-like), Lineage 5.1 (VR2332-like), and Lineage 3 (QYYZ-like) mixed in. FJLIUY-2017 also showed a complex recombination pattern involving these lineages.
One specific genetic feature they looked at was a deletion in a protein called NSP2. PRRSV2/CN/G8/2018 had a characteristic 131-amino acid deletion, just like NADC30-like strains, plus an *additional* 25-amino acid deletion. FJLIUY-2017 also had deletions, but they were different. These deletions are important because they can affect how the virus replicates and interacts with the host.
Putting the Viruses to the Test in Piglets
Okay, so they knew the genetic story. But the big question was: how pathogenic are they? To find this out, they did an animal study using young piglets that were confirmed to be free of PRRSV and other common pig diseases.
They divided the piglets into three groups:
- A control group (given a mock injection).
- A group inoculated with FJLIUY-2017.
- A group inoculated with PRRSV2/CN/G8/2018.
Each piglet in the infection groups got a dose of the virus, half up the nose and half injected into the muscle. Then, they watched the piglets closely for 14 days. They recorded:
- Rectal temperature (checking for fever).
- Clinical signs (coughing, lethargy, etc.) using a scoring system.
- Body weight (to see how well they were growing).
- Survival rate.
They also collected blood samples multiple times to check for:
- Viremia (how much virus was circulating in the blood).
- PRRSV-specific antibodies (the piglet’s immune response).
At the end of the study (or if a piglet died), they examined the lungs for gross lesions (what they looked like visually) and microscopic lesions (what they looked like under a microscope). They also checked for the presence of virus antigen in the lung tissue using a technique called immunohistochemistry (IHC).
What the Piglets Told Us
The results were quite clear and showed a significant difference between the two new strains.
The piglets infected with FJLIUY-2017 got pretty sick.
- They developed a persistent fever, often staying above 40.5°C for days.
- They showed more severe clinical signs like cough and lethargy.
- They had significantly lower weight gain compared to the control and the other infected group.
- Tragically, one piglet (20% of the group) died during the study period.
- They had high levels of virus in their blood (viremia), peaking early.
- They developed a strong antibody response quickly.
- Their lungs showed severe gross and microscopic lesions, typical of severe interstitial pneumonia.
- High levels of virus antigen were found in their lung tissues.
In contrast, the piglets infected with PRRSV2/CN/G8/2018 had a milder experience.
- They also developed fever, but it was less persistent and generally lower than the FJLIUY-2017 group.
- They showed only moderate clinical signs.
- Their weight gain was much better, similar to the control group.
- None of the piglets in this group died.
- They had lower levels of virus in their blood, and the peak viremia occurred later.
- Their antibody response was slower and lower.
- Their lungs showed moderate gross and microscopic lesions.
- Lower levels of virus antigen were detected in their lung tissues.
The control group piglets, as expected, stayed healthy with no fever, no clinical signs, good weight gain, no viremia, no antibodies, and healthy lungs.
Why the Difference? And What About Vaccines?
So, we have two recombinant viruses from similar lineage backgrounds, but one is clearly more pathogenic than the other. This study, along with others, really drives home the point that recombination among different PRRSV-2 lineages can create new variants, and some of these can be quite nasty.
The researchers also looked into why FJLIUY-2017 might be more virulent. They honed in on a specific protein, Nsp9, which is known to be linked to the severity of HP-PRRSV. They found that FJLIUY-2017 had specific amino acids (Serine at position 519 and Threonine at position 544) in its Nsp9 that are characteristic of highly pathogenic strains. PRRSV2/CN/G8/2018, on the other hand, had Serine at 519 but Alanine at 544, which is more like the NADC30 strain. This difference in Nsp9 might partly explain why FJLIUY-2017 caused more severe disease and mortality.
Now, what about vaccines? This is another big challenge. China uses various modified live virus (MLV) vaccines based on older strains (like Lineage 8 JXA1-R or Lineage 5 Ingelvac PRRS MLV). The study tested if antibodies generated by these common vaccine strains could neutralize the two new recombinant viruses. And guess what? They couldn’t effectively neutralize either FJLIUY-2017 or PRRSV2/CN/G8/2018. This is a major concern because it suggests that current vaccination strategies might not provide adequate protection against these newly emerging recombinant threats.
The Takeaway
What this study tells us is that PRRSV continues to evolve rapidly in China, driven by recombination between the different lineages circulating there. This process is spitting out new variants like FJLIUY-2017 and PRRSV2/CN/G8/2018, which can have varying levels of pathogenicity. The fact that FJLIUY-2017 caused significant disease and mortality in piglets, similar to highly pathogenic strains, is a serious warning sign.
Furthermore, the finding that current vaccine-induced antibodies didn’t neutralize these new strains highlights the urgent need for continuous surveillance and potentially updated vaccine strategies. The swine industry needs to be really vigilant about these evolving recombinant viruses because they pose a significant and ongoing threat to pig health and profitability. It’s a constant battle, and understanding these new players is the first step in fighting back.
Source: Springer
