Scientists Think Treatment for Common Cold Might Be a Step Closer After They Stopped Viruses From Replicating

Scientists hope a treatment for the common cold is a step closer after they stopped a virus from replicating under laboratory conditions.

The authors of a study published in the journal PLOS Biology hope their research could also help to wipe out illnesses like polio and viral meningitis.

The investigation looked at rhinoviruses and enteroviruses. Illnesses like the common cold, some sore throats, and certain types of pneumonia and bronchitis, fall under the rhinoviruses category. The echovirus and coxsackievirus—which both lurk in the digestive tract and can sometimes cause viral meningitis, as well as complications like pneumonia and hepatitis—are the most common forms of enteroviruses. Polio is another well-known, and potentially deadly, enterovirus.

Outbreaks of a condition called enterovirus 68 in the U.S. in 2014 and 2016 triggered severe respiratory illnesses in children, and was linked to cases of a rare spinal cord disorder, acute flaccid myelitis. At the moment, there are no antiviral drugs that can treat or prevent these types of illnesses.

Viruses are made up of DNA or RNA coated in protein. They cause illnesses by latching on to a host's cell, and hijacking its processes. This makes the cell replicate the genetic material of the virus. For this process to happen, the virus must change its shape.

The team tried to find a way to stabilize a part of the virus, to prevent it reshaping, releasing its genetic material and taking over host cells. So-called capsid-binder drugs, which slot into a pocket in some viruses and prevent it from invading the host cell, have been explored in the past. But viruses quickly become resistant to such approaches. Some only work against certain viruses, or don't have the pocket to begin with, the authors explained.

In their study, the scientists found a pocket on enteroviruses and rhinoviruses. They targeted it with compounds that stabilized an important part of the virus, stopping it from shape-shifting.

Study co-author Professor Sarah Butcher at the University of Helsinki explained to Newsweek the team tested how viruses grow in cell culture in a lab in the presence of many different molecules.

Next, they created computer models of the picornavirus—the family that rhinoviruses and enteroviruses are part of—to look where the drug might bind. They verified it using special equipment to watch this binding up close.

"We then went on to see which of the chemical properties of the molecules that bind were important so that better, more broad spectrum molecules could be found. We were able to stop the virus replicating," said Butcher.

They hope the pocket might be so important in the processes of virus replication that bugs that try to mutate and become resistant to drugs will end up too weak to spread.

Butcher explained antiviral research on this huge group of human pathogenic viruses has focused on research done 30 years ago on a druggable site on the bugs.

"Despite many trials, we still have no drug on the market to cure infection. This study shows that we have another druggable site which we found to be a mechanistic weakness of the virus that we can exploit," she said.

"It could help to cure the common cold, to help in combating the last cases of polio, and other diseases caused by entero and rhinoviruses," said Butcher.

However, she acknowledged molecules will need to be tailored to specific virus types.

"We also showed that the virus can mutate to escape the drug, but this normally made the resulting virus less fit. These are early days, and much work needs to be done before we will have a cure in the pharmacy."

The study marks the latest attempt by scientists to consign conditions like the common cold to history. Last year, scientists developed a molecule that blocked several strains of rhinovirus.

Researchers at Imperial College London created a molecule which targets a protein viruses latch onto to create a protective shell, enabling them to multiply. The molecule was found to work on human cells, but it will need to be replicated in animals and humans before it can be made into a treatment.

The findings were published in the journal Nature Chemistry.