Wouldn’t it be great if you couldn’t give someone else your cold? That might be possible sooner than thought, thanks to researchers at the Universities of Leeds and York.
According to their recent study, they have “for the first time identified the way viruses like the poliovirus and the common cold virus ‘package up’ their genetic code, allowing them to infect cells. The findings open up the possibility that drugs or anti-viral agents can be developed that would stop such infections.”
Once a cell is infected, the scientists wrote, a virus needs to spread its genetic material to other cells. This process involves the creation of virions — newly formed infectious copies of the virus. “Each virion is a protein shell containing a complete copy of the virus’ genetic code. The virions can then infect other cells and cause disease.”
What had been a mystery was a detailed understanding of how the virus assembles those virions.
“This study is extremely important because of the way it shifts our thinking about how we can control some viral diseases. If we can disrupt the mechanism of virion formation, then there is the potential to stop an infection in its tracks,” said professor Peter Stockley, former director of the Astbury Centre for Structural Molecular Biology at Leeds, who supervised the research with professor Reidun Twarock from York.
“Our analysis suggests that the molecular features that control the process of virion formation are genetically conserved, meaning they do not mutate easily — reducing the risk that the virus could change and make any new drugs ineffective,” Stockley said.
Their study, published January 8 in the journal Plos Pathogens, focused Enterovirus-E, which is the universally adopted surrogate for the poliovirus. It is a harmless bovine virus that is non-infectious in people. The poliovirus causes polio and is the target of a virus eradication initiative by the World Health Organization.
The enterovirus group also includes the human rhinovirus, which causes the common cold.
The study details the role of RNA packaging signals, which are short regions of the RNA molecule that — along with proteins from the virus’ casing — ensure formation of an infectious virion.
Using molecular and mathematical biology, the researchers identified possible sites on the RNA molecule that could act as packaging signals. Using advanced electron microscopes, they could see this process — the first time that has been possible with any virus of this type.
“Understanding in detail how this process works, and the fact that it appears conserved in an entire family of viral pathogens, will enable the pharmaceutical industry to develop anti-viral agents that can block these key interactions and prevent disease,” Twarock said.
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