- 20 minutes
- Expertise article
Parvovirus alert over changes and challenges
Pork producers and veterinarians need to be aware that the porcine parvovirus (PPV) has been evolving into new strains. A virus that was once thought to be genetically stable is now known to exist in a variety of forms, raising fresh questions about its control in sow herds.
The evolution of PPV and its implications for swine health management are discussed in a new Meet The Expert podcast from Boehringer Ingelheim, by Professor André Felipe Streck of the Institute of Biotechnology at the University of Caxias do Sul in southern Brazil.
Here is an extract from the podcast conversation, between Professor Streck and journalist Peter Best.
Q: Does PPV still need to be investigated, Professor Streck? After all, it is more than 50 years since it was shown to cause stillbirths, mummified piglets, embryonic death and infertility, while we have had parvovirus vaccines to use in our swine breeding herds for at least the last 40 years.
A: Yes, further investigation is necessary because the porcine parvovirus is changing. With Professor Uwe Truyen in Leipzig, Germany, we performed some studies focused mainly on evolutionary aspects of the virus and observed the occurrence and distribution of new antigenic types. In my opinion, new PPV vaccines are needed that may induce a greater immune response and cover all of the prevalent strains. I always say that the established PPV vaccines are still effective and we need to practise regular vaccination, but the process of vaccine product improvement should be continuous since we see that the virus also has a continuous evolution.
Q: We should remind ourselves how and where PPV infection is seen in practice.
A: The only well established clinical sign of a PPV infection is maternal reproductive failure. In sows and gilts the important sign is mummification. At the embryo stage in early gestation, infection can result in embryonic death followed by reabsorption of fluids and the soft tissues. From Day 35 on, though, there can be mummification of a dead foetus. By 70 days of gestation, the foetuses already have some immune system and may resist virus infection. In infected litters it is common that not all foetuses are affected in the same way. Many times we have seen mummification in only a few foetuses and others in the litter manage to survive. When you see litters such as from first-parity gilts, in which there are some mummified foetuses along with stillborn pigs and healthy, live piglets, that’s the big hallmark of porcine parvovirus.
Q: Have there been significant developments in PPV diagnosis in recent years?
A: The big difference with diagnosis of PPV came when we started to perform PCR for it in the 90's. That helped us a lot to discover new strains. Recently, the use of real-time PCRs has been important for showing the amount of DNA of this virus. With the technique we can establish whether PPV was the primary cause of this mummification.
Q: You mentioned discovering new strains, have there been significant genetic changes in the virus since PPV was first reported in the mid-60’s?
A: The main divergence of this virus was introduced in the last 40 years. Most importantly, in recent years, new amino acids have been found in the external capsid, the part of the virus that has contact with the immune system of the host. In other words, we can see new antigenic profiles of this virus. These antigenic profiles were observed in strains from several countries, mostly in Europe.
Q: This genetic divergence that we see today, with its roots going far back, was it evolution by mutation?
Yes, mutation drives this evolutionary process of parvovirus. Although it is a DNA virus, we can estimate for PPV a very high mutation rate or substitution rate. In the past it was considered more stable than other viruses, with a substitution rate or mutation rate close to that of the host. This was because it uses host polymerase for replication and the polymerase complex in animal cells acts as a repair unit. But for some reason, in the parvovirus the repair unit doesn't work so well, the polymerase acts more like in an RNA virus and inserts a lot of mutations in the DNA sequence.
Q: Why was there the original idea of PPV being a stable virus?
A: Looking back, probably two reasons explained why PPV was not a huge problem at the time. First, vaccination was very effective. Second, the diagnostic techniques available then were not so sensitive, making it much more difficult to reach a diagnosis about a mummified foetus.
Q: What has that process of evolution produced today, multiple strains and genotypes from country to country?
A: Some genetic variability was observed in PPV from strains from Brazil in the 90’s, involving mutations mainly in the virus shell or capsid and allocated to two phylogenetic groups. Subsequently, studies from Professor Truyen in Germany saw two other phylogenetic clusters, in which there was the start of a predominance of the 27a strains. Other studies afterwards also found new clusters and 27a-like strains in different continents, such as in China, as well as in European locations including Austria and Romania.
Q: What's different about the strain called 27a that was isolated originally in Germany? Does 27a differ both genetically and antigenically?
A: In fact I prefer now to talk about 27a-like strains because the original 27a maybe does not exist any more. They differ because they have some new amino acids located in a very important part of the capsid. We call these locations ‘loops’ and they are exactly the parts that stimulate the immune system. The changes in some points of these loops can have other effects, like a better replication activity of these strains. This way, the 27a-like strains are very important in the field.
Q: You mention antigenic differences. Is a 27a-like PPV generally more virulent?
A: That's a nice question. Studies by Professor Truyen did see that 27a was more virulent, compared to a more standard PPV virus. Importantly, the variants could replicate better in some cases and antibodies raised against some older strains have some reduced neutralising capability against these 27a strains.
Q: Is this PPV evolution an international phenomenon?
A: Mostly so far these 27a-like strains occur in Europe and the Americas. Reports from Asia are isolated by comparison. For some Asian countries like China we observe a predominance of other strains and a greater diversity of the strains there. In Europe, while 27a-like PPV predominates in sow herds, the strains in wild boar populations are genetically more diverse.
Q: Has this emergence of new variants coincided with an increase in submissions to diagnostic laboratories involving porcine parvovirus?
A: Yes, here in Brazil, we can observe a higher incidence in positive cases of porcine parvovirus and of mummification in our herds. Talking to colleagues from other countries, it is seen there as well. Usually we observe PPV in, say, 30-40 percent of our foetuses. That's a very huge number of incidents, especially if we remember that some diagnoses gave false negative results because the mummified samples reaching the laboratory were too autolysed. To test a mummified foetus you need someone to collect the foetus and bring it immediately to a freezer, then send it quickly to the lab. Sometimes this process can take some days or even some several weeks to perform, which can mean a foetus arrives in a condition that is no longer good for testing.
Q: Could our use of established vaccines have played a role in influencing the evolution of the parvovirus?
A: We don't need to blame the vaccine for these new mutants or new strains. An early hypothesis was that the emergence of new capsid profiles could be due to viral adaptation towards vaccines. These strains were sometimes called escaped mutants. However, in our studies we could see how a very adapted strain could manage to stand out from others because it was more fit to compete with them. Vaccination could even reduce some genetic diversity. Genetic variability usually occurs when the virus has a little bit more freedom to replicate, which doesn’t happen when you have a vaccine. Vaccinating imposes serious selective pressure on the predominance of certain strains. That’s why it's important to monitor wild boar populations, which don't have vaccines and therefore usually have a higher genetic diversity for porcine parvovirus and other viruses.
Q: All the evidence tells us that porcine parvovirus occurs in at least two-thirds of sow herds in just about every country where pigs are produced. We can't really think about stamping it out, therefore we must live with it. In practice today, what’s needed to a protect a sow herd against PPV?
A: First, vaccination must be continued. Here in Brazil, swine producers only vaccinate when they have cases of mummification. After a while they stop the vaccination again. Obviously, this causes a great circulation of the virus in their herds and the risk of reproductive failure. Second, in addition to the further development of vaccine technology and new technologies for the diagnostics of parvo, we must always monitor the field strains to understand the relationship with the vaccine used and also with pathogens. With this, we will be one step ahead of new infections.
Q: You view new vaccine developments as welcome, to take account of the emergence of different dominant virus strains in pig populations and the response that they might have to the traditional vaccines?
A: The improvement of vaccine technology must be constant. We have to keep in mind that this virus has a high mutation rate and will never stop undergoing changes. I also highlight the importance of monitoring these changes, in countries with large swine production systems. This evolutionary process is geographically related and therefore the vaccine companies as well as swine producers and veterinarians must be aware of the information.
