African Swine Fever (ASF) is devastating the China swine industry since its introduction several months ago. There is no real end in sight as the virus continues to spread by contaminated trucks that visit slaughterhouses and farms. These contaminated trucks move about freely from farm to farm without sanitation or appropriate disinfection. Since there is no treatment for ASF and the mortality is very high, essentially reaching about 100%, it is natural that people should seek a vaccine that can stop this marauder. The history of ASF and similar diseases suggests that host immunity is not important in stopping this disease, and furthermore it may not be desirable to vaccinate, not even in the short term.
History of ASF
African Swine Fever is thought to have arisen in the tick and wild suid population about 1700 AD. The wild suids and the local tick and the ASF virus became adapted to each other to some extent and the ASF virus causes little if any mortality among the well adapted wild suid. ASF has been generally known in the world since its first major outbreak in Kenya in the 1920s.
At that time the cattle disease Rinderpest had been wiping out the cattle in Kenya and the British colonials wanted for meat so they hit on the idea of introducing pigs. But as soon as their pigs met up with the local wild suids (wart hogs, bushhogs, forest hogs), and the local ticks, their pigs began to die off rapidly. At first Classical Swine Fever was suspected but later it was learned that a new deadly disease had been encountered. CSF is a RNA virus similar to some viruses causing disease in ruminants, while the ASF virus is a completely unique DNA virus with no phylogenetic relationship to CSF.
The relatively low population densities of pigs in mostly undeveloped Africa kept the disease mostly confined to the southern realms of Africa. Any contact with naive domestic pigs would wipe them out totally and there was no significant spread and not much generation to generation transmission among domestic pigs. But as the central regions of Africa developed in the 1900’s there were more opportunities for the meat and cast offs of ASF infected pigs to be carried further and further north by man.
After 1920, ASF gradually marched northward reaching north Africa and the Mediterranean a few tens of years later, not because ticks went slowly, diligently, tireless crawling northward toward Europe, but because man was moving the virus by his activities, and the virus was moved all the way to Europe by 1957. There was a massive outbreak of African Swine Fever in Cuba in 1971 which was controlled by mass depopulation of infected and in-contact swine. (Cuba is also infected with Classical Swine Fever, which remains endemic in Cuba.)
ASF Types -
Type II (type two) ASF causes an acute form of the disease with high mortality approaching 100% among all ages of domestic swine.. Type I ASF produces a milder more chronic form of the disease. Pigs infected with Type I ASF tend to resist infection with type II. Much current vaccine-oriented research seeks to develop a modified live vaccine based on attenuated strains of type I that will protect pigs while avoiding the severe debilitating chronic disease seen with type I ASF. No vaccine safe enough to use in pigs has been found. Attempts to modify the virus to make it safe for pigs destroys the ability to protect the pigs. Killed vaccines have failed.
The Classical Swine Fever Experience - Persistent Infections
Prior to about the end of World War 1, “Swine Fever” (now called Classical Swine Fever to differentiate it from ASF) was wreaking mass havoc on the pig industry worldwide. In the early days of CSF ("Hog Cholera") an outbreak could easily amount to thousands of dead hogs, one outfit in Indiana famously losing over 10,000 head in a single month in 1887. More than 13% of the pigs in the US died from CSF in that year. Many countries decided to eradicate CSF and after many fitful attempts to control CSF by various vaccination strategies, the disease was eradicated in the UK in 1966 and from the US about 1975. An immunization strategy using immune serum from pigs and live hot virus administered simultaneously was popular in the USA for many decades. The use of serial passage in rabbits was used in the 1940's to make a somewhat successful modified live vaccine. This “lapinization” (passage in rabbits) technique was used by European and Asian researchers and various MLV vaccines were introduced in the 1950s including the popular C-strain vaccine still produced and used in China since 1954. Modern subunit technologies developed over 20 years ago are being used to design E2 protein vaccines that gradually supersede the obsolete and problematic C-strain MLV vaccines.
If one has worked in the Chinese swine industry for any length of time, and has been even half-awake and learned anything at all about Classical Swine Fever -- the first lesson on CSF in this "College of Hard Knocks" is -- that the beloved C-strain vaccine may indeed perform beautifully in carefully controlled studies under laboratory conditions, but c-strain does not work quite so well in the field. Out here in the fields, the serious forms of CSF with massive pig die-offs are controlled fairly well by c-strain vaccination, but the so-called atypical and chronic forms of verticallly transmitted CSF disease have become the common form, and occasionally large enough "critical masses" of virus and susceptible pigs result in alarmingly high mortality CSF outbreaks even in the face of vaccination with "good vaccine", handled properly, administered in timely fashion. The C-strain vaccine often fails.
At a meeting in Nanjing a couple of years ago a panel of Chinese veterinary experts agreed that Classical Swine Fever was the number one (#1) problem facing the swine industry, despite 60 years of c-strain vaccination. One should not say that the c-strain vaccine has been unsuccessful – the annual sales volume is about USD$300 million year after year after year… Countries that have eliminated CSF do quit vaccinating. In the modern case, the E2 subunit vaccine is used until eradication is realized. Cuba reports that C-strain vaccination has resulted in chronic CSF, similar to the China experience. The Chinese pig industry has established a program for the eradication of CSF rather than "vaccinate and live with the problem".
Not "Real Immunity" to ASF Even after Natural Infection
Not every pig that becomes infected with ASF type II will die, although more than 95% generally do. What about those that survive? The pig that survives ASF infection continues to shed the virus and can pass the disease onto other pigs. In other words, the surviving ASF pig does not have what some classify as true immunity with elimination of the invading virus but what is called “premunition”, a state in which the animal is not killed by the virus but also cannot eliminate the infection. Premunition is also referred to as “persistent infection” or PI. In the case of CSF, the disease is maintained in the pig population by persistent infection. The word “Premunition” is a French word coined by the veterinary researcher G. Parrot in 1937 to describe the situation where there is enough resistance in the host to avoid mortality but not full recovery and sufficient immunity to expel the virus.
Given the genetic complexity of the ASF virus, the situation of pig production in China, and the experience with CSF and other viruses, it seems that the most likely outcome of vaccination against ASF is not “true immunity” but rather “premunition” and “Persistent Infections”. Persistent infection is rather the norm among many serious virus infections. If there is no PI, the virus burns itself out of a home and disappears. ASF is the sort of virus that sticks around, and vaccination will help it to do just that. A decision to vaccinate is a decision to live with ASF. We will be much better off to get rid of ASF rather than try to live with it.
Eradication is the best solution for the future of the pig business.
Parrot, G. 1937.
Les rickettsioses conférent-elles l'immunite vraie pu la prémunition?
Arch Inst Pasteur d’Algerie. 15 (2) pp.188-213.
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