The common cold could potentially become a thing of the past now that a group of researchers from the U.K. has cracked the code that governs the virus responsible for this infection.
The breakthrough could mean a possibility to stop virus molecules from replicating by stopping them from transmitting the instructions that are needed so they can copy and multiple themselves.
For the new study, which was published in the Proceedings of the National Academy of Sciences (PNAS) on Feb. 2, Peter Stockley, from the Faculty of Biological Sciences at the University of Leeds in the U.K., and colleagues used a computer-based model to identify the code in the viral genome that causes rhinoviruses, a group of viruses responsible for most colds.
The researchers found a hidden code within the sequence of the virus' ribonucleic acid (RNA). They likewise found that jamming this code can cause disruption in the virus assembly, which can stop it from functioning and thus prevent disease.
Stockley likened their discovery to an Enigma machine that allows researchers to see how the viruses are deployed and which could be crucial to winning the war against the common cold.
"Now, for this whole class of viruses, we have found the 'Enigma machine' -- the coding system that was hiding these signals from us," Stockley said. "We have shown that not only can we read these messages but we can jam them and stop the virus' deployment." The Enigma machine refers to a German cipher machine used before and during World War II to code and decode messages.
Although single-stranded RNA viruses are the simplest of viruses and were likely one of the earliest to evolve, they are still one of the most potent and harmful pathogens with the rhinovirus, which is responsible for the common cold, being accountable for about 1 billion infections every year.
Other single-stranded RNA viruses also include those responsible for HIV and Hepatitis C and the discovery could pave way for improved treatment for these conditions.
Study researcher Roman Tuma, from the University of Leeds, said their study also demonstrates the possibility of designing molecules that can interfere with this newly discovered code so it could no longer be interpreted and in the process will effectively stop the virus in its tracks.
"Packaging signals overlap untranslated and coding regions ensuring assembly is in competition with other functions of the genome," the researchers wrote. "Disrupting these contacts has deleterious consequences for capsid assembly identifying a novel antiviral drug target."
