Genome research aids understanding of killer Schmallenberg virus
Researchers have developed methods to synthesise and change the genome of the Schmallenberg Virus, in a bid to understand how it induces disease among livestock.
The research, led by Massimo Palmarini and Alain Kohl at the MRC Centre for Virus Research at the University of Glasgow, has laid bare important ways by which the Schmallenberg virus causes disease and has paved the way for future development of new vaccines.
Schmallenberg has spread rapidly throughout Europe since its discovery in Germany in October 2011.
Professor Palmarini said: "Insect-borne viruses, known as arboviruses, are increasingly becoming a problem throughout the world, whereas years ago they were limited mainly to the tropical areas of the globe. The spread of arboviruses is probably the result of several factors, including increase in travelling and commercial exchanges, climate and ecological changes, and increased livestock production.
"This study will help us to understand how Schmallenberg virus works, but it can also serve as an example for other related viruses that may emerge in the future."
The new research describes the molecular biological methods used to design and assemble the viral genome completely in a test tube in a form that can be easily introduced and replicated in cultured cells. From these cells the researchers recovered the virus with identical infection properties to the natural Schmallenberg.
This approach, known as "reverse genetics", allowed them to control the viral genome and identify a gene involved in protecting the virus against the immune response of infected animals.
The researchers then made viruses missing the gene. They discovered that, without the gene, the virus adversely affected mice in the laboratory less than the virus containing the gene. Researchers also discovered that the virus rapidly grows in the brain and spinal cord of aborted lambs and calves. It prefers to infect neuron cells, which explains why it infects and damages the brain. This also results in muscular defects such as abnormally flexed legs often seen in stillborn animals when the virus is transmitted from an infected mother to the calves or lambs in the uterus during pregnancy.