October 15, 2019
Disabling a single, apparently noncritical protein in cells may deter the replication of viruses known to cause 50% f all common colds—as well as polio, asthma, encephalitis, and other diseases—according to researchers at Stanford University and UC-San Francisco.
Few of us escape without catching at least one rhinovirus during the winter—when germs breed freely in closed environments. 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.
The recent academic findings about cold prevention were made in human cell cultures and in mice.
“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 Jan Carette, associate professor of Microbiology and Immunology at Stanford. “Now we have a new way to do that.”
In a study published online in the September 16 edition of Nature Microbiology, Carette and his associates found a 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 tha tall enteroviruses appear to need in order to replicate.
Carette shares senior authorship with Or Gozani, MD, PhD, professor of biology at Stanford and the Dr. Morris Herzstein Professor of Biology; Raul Andino, PhD, professor of microbiology and immunology at UCSF; and Nevan Krogan, PhD, professor of cellular and molecular pharmacology at UCSF. The lead authors are former Stanford graduate student Jonathan Diep, PhD, and Stanford postdoctoral scholars Yaw Shin Ooi, PhD, and Alex Wilkinson, PhD.
Research contact: @Stanford