According to a study published September 16, 2019, in the journal Nature Microbiology, researchers at Stanford University and the University of California in San Francisco found that temporarily disabling a single, noncritical protein in cells (called methyltransferase SETD3) could halt the duplication of viruses, including the rhinovirus that causes most common colds. Switching off the protein in human cells and in mice also stopped replication of viruses linked to asthma, encephalitis, and polio. Microbiologists targeted a human gene that produces a protein essential to the function of numerous enteroviruses (including rhinoviruses).
How Host-Directed Therapy Works
Traditional antiviral drugs target the virus itself. But there are about 160 known types of human rhinoviruses (HRVs). That “remarkable phenotypic diversity,” the study’s authors write, “has precluded development of a vaccine and effective antivirals.” RELATED: Cold and Flu 101 A different antiviral approach, known as host-directed therapy (HDT), targets host-cell proteins that viruses need in order to replicate and cause infection. “In this study, the investigators have done something very clever,” says William Schaffner, MD, an infectious disease specialist and a professor of preventive medicine and health policy at the Vanderbilt University School of Medicine in Nashville, Tennessee, who was not involved in the study. “Pretending the cold virus is a key trying to get into the lock [referring to the host cell], researchers have disabled a protein on the cell so the virus cannot infect those cells.”
A New Weapon Against the Common Cold’s Impact on Society
“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?’” said the study’s senior author, Jan Carette, PhD, an associate professor of microbiology and immunology at Stanford, in a press release. “Now we have a new way to do that.” While this is a preliminary study, Dr. Schaffner believes it is a very promising development. “Long journeys begin with first steps,” he says. “This gives us hope that we can develop a drug with broad antiviral activity against not only the common cold but maybe all enteroviruses, without even disturbing SETD3’s regular function in our cells,” Dr. Carette said. “Common colds have a strong economic and social impact in our society, keeping people away from work and school,” says Schaffner. “There is great interest in the next stages of research that will open up possibilities that this trial may work in people.”
