A recent study published in the Journal of Virology theorized that the common cold virus crossed the species barrier into humans from birds nearly 200 years ago. The researchers hoped that a retrospective understanding of the enterovirus’ pathology could staff effective methods of eradicating it completely in the future.
“Besides the evolutionary history of metapneumoviruses, we also investigated the mutation rates and the selection pressures of these viruses. An understanding of how viruses evolve and how they adapt to new hosts and their immune systems is important, especially if we are to prepare for new, potentially pandemic diseases,” explained contributing author Dr. Ron Fouchier.
Identifying the host
You might recall, that Fouchier and his colleagues achieved a fair share of infamy after modifying a deadly avian H5N1 influenza virus in rodents in the service of an in-depth study on pathogens. The rate at which these viruses are able to replicate and mutate shield them from many prospects of practical experimentation.
It’s a conundrum that has plagued the medical community for years even if few comprehend how layered the puzzle actually is. The virus frequently referred to as the common cold, isn’t just one virus, but a varied horde of stains. There are roughly 160 rhinovirus infections that inform the symptoms associated with the century-old affliction-all of which are particularly adaptable in the face of drug treatment. Their mutations enable them to dip past our immune system fairly easily and spread with malicious abandon.
The only way to cure a mutating drug-resistant alien is by precluding its replication. A team of researchers from Stanford and the University of California, are confident that they have done exactly that. The new study published in the journal Nature Microbiology extracts an element that all of the strains depend on to spread successfully.
“Most cases of the common cold are caused by rhinoviruses. There are more than 150 types of this virus. A typical vaccine like the influenza vaccine contains at most four types, so making it for all 150 strains would be extremely challenging,” Jan Carette, coauthor of the new study and Ph.D., associate professor of microbiology and immunology explained in a statement. “We have identified a single human protein that helps the common cold virus to replicate and spread. Inactivating this protein could be a new strategy to prevent colds.”
As previously stated, employing vaccination for each strain wouldn’t work because in addition to being extremely diverse the pathogens are also prone to mutations. Given this, the researchers opted instead to hone in on a protein called SETD3, which has been observed to be essential to viral success.
After producing a culture of human cells that did not have said protein, they infected them with a range of enteroviruses-none of these could successfully replicate under these conditions. The team attempted the same experiment on a crop of mice and not only did they successfully duplicate the results, but this approach was also effective against viruses linked to asthma, encephalitis, and polio.
“This gives us hope that we can develop a drug with broad antiviral activity against not only the common cold but maybe all enteroviruses,” Carette concluded, “without even disturbing SETD3’s regular function in our cells.”