The paper of scientists at the University of California, Riverside, reflects a major step forward in the study of how some of the world’s most virulent viruses, such as West Nile, SARS, Ebola and Hepatitis C interact with their hosts.
“All these viruses are very dangerous and are traditionally studied in animal models, so large-scale genetic studies of the host-virus interaction is very hard to do,” said Shou-Wei Ding, who works in the Center for Plant Cell Biology at UCR’s Institute for Integrative Genome Biology. “Needless to say, we are all very excited to find that this little worm can be used to understand how hosts genetically control viruses.”
For years researchers throughout the world have studied C. elegans because many aspects of its biology, such as genetics, development and the workings of neurons, mirror the biology of humans. However, no viruses were known to infect the millimeter-long roundworm so it was not used as a model for studying viral infections.
The UC Riverside researchers have developed a strain of the worm, in which an animal virus could replicate, allowing them to map the delicate dance of action and reaction between virus and host.
The UCR team has shown that virus replication in the worm triggers an antiviral response known as RNA silencing or RNA interference (RNAi). RNAi specifically breaks down the virus’ RNA. Virus RNA creates proteins that allow the virus to function. The virus responds by producing a protein acting as a suppressor of RNAi to shut down the host’s antiviral response. Virus infection did not occur when the viral RNAi suppressor was made inactive by genetic mutations in the host system.
C. elegans’ RNAi system is considered a “blanket system,” meaning that it has parallels in humans, making the worm model discovered by Ding and his colleagues a valuable tool in studying the way viruses interact with hosts. This tool may speed the discovery of treatments for virus-caused diseases that plague humans.
MEDICA.de; Source: The University of California, Riverside