Spironolactone, commonly used in cases of heart failure, has surprised scientists by blocking infection by Epstein-Barr virus, in a breakthrough that could help people with a wide variety of herpes-related conditions.
In 1996, Medical Microbiology reported that there were over 100 known herpes viruses, eight of which can normally affect humans.
Herpes simplex virus type 1 (HSV-1) is transmitted by mouth and causes cold sores. HSV-2 is responsible for genital herpes, causing painful blisters or ulcers in the genital area. HSV-3, or herpes zoster, leads to chicken pox and potentially shingles.
HSV-4, also called Epstein-Barr virus (EBV) is responsible for infectious mononucleosis, commonly known as glandular fever or “kissing disease,” because it spreads through saliva.
EBV has also been linked to a number of other conditions, including cancers in humans. People who undergo a transplant, or whose immune system is already compromised, are especially at risk of EBV.
According to the authors of the current study, EBV “infects the majority of humans worldwide.” The Centers for Disease Control and Prevention (CDC) call it “one of the most common human viruses in the world.” Most people, they say, will have this virus, but often there are no symptoms.
There is only one class of antiviral medicine to treat herpes viruses, which means there is no alternative in cases of resistance.
Scientists from the University of Utah School of Medicine, led by Dr. Sankar Swaminathan, have been searching for new drugs to treat viral infections. They were screening for drugs that might be effective against the herpes virus through a different mechanism than currently available therapies.
The current drugs work by preventing a virus from replicating DNA, thus blocking a middle step of the viral infection cycle.
Spironolactone (SPR), like existing drugs, was found to block a key step in viral infection that features in all herpes viruses, but a different step than the one targeted by current drugs. It prevented replication of the virus in cells by blocking the so-called SM protein, needed for a late step in the infection cycle.
Based on these findings, the researchers see SPR as a good candidate for development into a new class of anti-herpes drug.
Dr. Swaminathan, who is chief of infectious diseases at University of Utah Health Care and professor of internal medicine, comments:
“It’s remarkable that a drug we have used safely in the clinic for over 50 years is also an effective EBV inhibitor. It goes to show how basic research can reveal things we would never have found otherwise.”
SPR is normally used to treat heart failure through a metabolic mechanism, but in dealing with viral infection, a different pathway appears to be at work.
The authors of the current study found that a drug similar to SPR has a similar ability to treat heart failure but does not affect the development of the herpes virus. These results suggest that the actions of spironolactone are separable.
Since all herpes viruses depend on SM-like proteins to spread infection, the results have broad implications.
The researchers envisage SPR becoming a template for a new class of drug to treat all herpesviruses. They believe it can be modified to work as an antiviral without adverse effects, and that it can help in the fight against drug-resistant infections.
Medical News Today recently reported that the herpes virus may contribute to cognitive decline.