Speeding up mutation is emerging as a potential new way to treat virus infection. Now, a new study shows that favipiravir – a trial drug currently being tested against Ebola and influenza – successfully treated norovirus in mice using that method.
Norovirus, also known as “winter vomiting bug” or “stomach flu,” is the most common cause of acute gastroenteritis in the US, where every year it causes 19-21 million illnesses and contributes to 56-71,000 hospitalizations and 570-800 deaths. The virus is also responsible for most foodborne-disease outbreaks in the US.
Norovirus is extremely contagious; you can get it from contaminated food or water, an infected person or by touching contaminated surfaces. The virus causes acute gastroenteritis, where the stomach or intestines – or both – get inflamed, leading to symptoms such as stomach pain, nausea, diarrhea and vomiting.
Most people who become infected experience an unpleasant but short-lived illness, but people with weak immune systems can become chronically infected for years and experience major health problems. Currently, there is no vaccine or treatment for norovirus.
Norovirus is difficult to study because it does not grow efficiently in the laboratory. The virus belongs to a class known as RNA viruses because their genetic material is made of ribonucleic acid (RNA). Most viruses that cause epidemics are RNA viruses, including Ebola, influenza, SARS and polio.
RNA viruses are a challenge for vaccine and treatment developers because they mutate and replicate rapidly.
Now, in a new study published in the journal eLife, a team at Cambridge University in the UK has shown that the experimental broad-range antiviral favipiravir, currently being trialled for influenza and Ebola viruses, effectively reduced – and in some cases eliminated – norovirus in mice.
Their work shows that favipiravir is effective at reducing norovirus in the body and in feces, which may help reduce disease severity and onward transmission.
In their study, the team shows how by speeding up mutation in the virus, the drug induces errors to develop in the viral genetic code. And, since the virus also replicates rapidly, these errors quickly accumulate and take hold, eventually preventing further replication and spread.
Dr. Armando Arias, a researcher in the lab of Ian Goodfellow, senior author and professor in the department of pathology at Cambridge, says:
“Our work in mice is very promising and shows that the drug favipiravir can make the virus mutate itself to death.”
The authors say this is the first time someone has shown you can fight a virus by making it mutate itself to death in the host. They suggest it may be possible to fight other RNA viruses in the same way.
Professor Goodfellow, a Wellcome Trust senior fellow, says most people will have been infected with norovirus at some point and experienced it as an unpleasant but mild illness that can be treated by drinking plenty of fluids and riding it out.
“But some patients get infections that can last months or years, and this has a real impact on their quality of life,” he adds. “The ease with which infections spread, particularly in places such as hospitals, schools and cruise ships, and the potentially serious health problems norovirus can cause people with weakened immune systems means that we desperately need a way to treat infection.”
Dr. Arias says as well as treating infected individuals, “the drug may also be useful in preventing infection during an outbreak. The next steps will be to test whether this drug is safe and effective at treating patients, too.”
The study was funded by the Wellcome Trust.
In June 2014, Medical News Today reported how, after conducting the largest ever review of noroviruses and acute gastroenteritis, the Centers for Disease Control and Prevention (CDC) found estimates are higher than previously thought, highlighting the need for norovirus vaccines.