New approach: researchers were able to stop the common cold
According to health experts, the common cold is the most common infectious disease worldwide. But although so many people are affected, the disease is still not curable. Only the symptoms can be treated. But researchers from the United States are now reporting that they have found a way to stop colds and infections with closely related viruses.
Temporarily deactivating a single protein in our cells could protect us from colds and other viral diseases. This is the result of a study carried out by researchers from Stanford University and the University of California-San Francisco. According to a message, the findings were made in human cell cultures and in mice.
"Complete protection" achieved
"Our grandmothers always asked us: If you're so smart, why haven't you found a cure for the common cold?" Said Prof. Jan Carette of Stanford University. Now they have found a new way to treat the condition. Instead of attacking them directly, the researchers aimed at an essential protein in our cells that the viruses have to replicate. The approach resulted in "complete protection" in experiments on mice and human lung cells, reports the "BBC". He also helped stop viruses associated with asthma, encephalitis and polio, the release said.
Colds are often triggered by rhinoviruses
At least half of all colds are caused by rhinoviruses. There are around 160 known rhinovirus types, which explains why you can quickly get infected again after a cold. To make matters worse, rhinoviruses are highly susceptible to mutations and, as a result, quickly develop drug resistance and escape immune monitoring caused by previous exposure or a vaccine.
In the study now published in the journal "Nature Microbiology", Carette and his team found a way to prevent a wide range of enteroviruses, including rhinoviruses, from replicating in human cells in culture and in mice. They did this by deactivating a protein in mammalian cells that all enteroviruses seem to need for replication.
Known and feared
One of the best known and most feared enteroviruses is the poliovirus. Until the introduction of an effective vaccine in the 1950s, the virus paralyzed and killed thousands of children every year in the United States alone. Since 2014, another type of enterovirus, EV-D68, has been involved in mysterious outbreaks of a polio-like disease, acute flaccid myelitis, in the United States and Europe. Other enteroviruses can cause encephalitis (inflammation of the brain) and myocarditis (inflammation of the heart muscle).
Very strong reduction in virus replication
Enteroviruses - like all viruses - can move around easily. For replication, they use proteins in the cells that infect them. The US researchers have now found one of the components on which the viruses depended. Scientists started with human cells and used genome editing to deactivate a single gene in each of the cells. These modified cells were then infected with RV-C15, a rhinovirus known to worsen children's asthma, and then EV-C68, which is involved in acute flaccid myelitis.
All of these viruses were unable to replicate in cells where the functions for a protein called SETD3 were turned off. "It was clearly critical to viral success, but not much was known about it," said Carette. The researchers observed a 1,000-fold reduction in virus replication in human cells without SETD3 compared to those with the protein.
The scientists then developed genetically modified mice that were unable to produce this protein at all. "The lack of this gene completely protected the mice from a viral infection," Stanford's Carette told the BBC. "These mice would always die [without the mutation], but they survived and we saw a very strong reduction in virus replication and a very strong protection." The animals grew into adulthood and were fertile.
Hope for a drug
It is not planned to produce genetically modified people, but to find a drug that temporarily suppresses and protects the protein. The study results "give us hope that we can develop a drug with broad antiviral activity not only against colds but possibly against all enteroviruses without affecting the regular function of SETD3 in our cells," said Carette. "I think the development can go relatively quickly." The role of the protein in virus replication is still uncertain and requires further investigation.
The viruses may not be kept in check for long
Prof. Jonathan Ball, a virologist at the University of Nottingham (UK), who was not involved in the work, said the study was "orderly", but scientists had to be sure that the approach was safe. "There is increasing interest in the development of therapies that target these host proteins because they may be able to overcome the virus mutation - one of the main obstacles to the development of effective, broadly effective antivirals," said the expert. "But viruses are of course very adaptable and it is conceivable that they will not be kept in check for long even by treatment directed at the host." (Ad)
Author and source information
This text corresponds to the specifications of the medical literature, medical guidelines and current studies and has been checked by medical doctors.
- Stanford University: In human cells and mice, a cure for the common cold, Stanford-UCSF study reports, (accessed: September 17, 2019), Stanford University
- Nature Microbiology: Enterovirus pathogenesis requires the host methyltransferase SETD3, (accessed: September 17, 2019), Nature Microbiology
- BBC: Common cold stopped by experimental approach, (accessed: September 17, 2019), BBC