Scientists found a sneaky way to stop cold viruses from replicating in mammalian cells by disabling a protein not in the virus but in the cells they infect.
By Bruce Goldman
"Our grandmas have always been asking us, 'If you're so smart, why haven't you come up with a cure for the common cold?'" Stanford virologist Jan Carette, PhD, told me a couple of weeks ago. "Now we have a new way to do that."
Carette's comment came in the course of filling me in on recent discoveries in his lab, in collaboration with University of California-San Francisco researchers, that are detailed in a new study published in Nature Microbiology.
Colds, or noninfluenza-related upper respiratory infections, are for the most part a weeklong nuisance. They're also the world's most common infectious illness, costing the United States economy an estimated $40 billion a year.
At least half of all colds are the result of rhinovirus infections. There are roughly 160 known types of rhinovirus, which helps to explain why getting a cold doesn't stop you from getting another one a month later. Making matters worse, rhinoviruses are highly mutation-prone and, as a result, quick to develop drug resistance, as well as to evade the immune surveillance brought about by previous exposure or a vaccine.
Rhinoviruses belong to a genus called enterovirus. Like all viruses, enteroviruses travel very lightly. Packing only their bare-minimum essentials inside their surrounding hard-shell protein capsids, these crafty infectors take advantage of proteins present in the cells they've checked into with procreational intent.
Enteroviruses do a lot more than make our noses run. One of the most well-known and feared enteroviruses is poliovirus. Until the advent of an effective vaccine in the 1950s, the virus spelled paralysis and death for many thousands of children each year in the United States alone. Since 2014, another type of enterovirus, EV-D68, has been implicated in puzzling biennial bursts of a polio-like disease, acute flaccid myelitis (AML), in the United States and Europe. Other enteroviruses can cause encephalitis and myocarditis -- inflammation of the brain and the heart, respectively.
Carette and his associates found a sneaky way to stop a broad range of enteroviruses, including rhinoviruses, from replicating inside human cells in culture, as well as in mice. They accomplished this feat by disabling a protein, in mammalian cells, that all enteroviruses appear to need in order to replicate. This protein appears to be nonessential to us humans, at least in the short run; so the idea is that knocking it out for a week or so -- long enough to send Rhinovirus, Inc., packing -- might not cause any noticeable side effects, although that remains to be proven.
The same approach of targeting a protein in our own cells also worked to stop viruses associated with asthma, encephalitis, myocarditis, polio and AML.
"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 said.
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