EXCLUSIVE Experts finally find treatment for incurable viral infection suffered by 122million Americans
Half of Americans are suffering from an incurable disease that causes painful - and embarrassing - blisters and sores around the mouth.
About 122million people have herpes simplex virus 1 (HSV-1), the oral strain of herpes. It's spread though close skin-to-skin contact and differs from the sexually transmitted herpes simplex virus 2 (HSV-2), which causes genital blisters and sores.
There is no cure for HSV-1, but antiviral medications can manage outbreaks and reduce the risk of transmission.
Now, however, researchers from Spain, have discovered how the virus acts on a person's DNA, opening the door for a possible cure.
The team found that the virus 'hijacks' a certain enzyme in the body that allows herpes to replicate itself, but if that enzyme is blocked, it brings 'the hostile takeover to a halt.'
The researchers are hopeful that the study's findings, which provide the first proof herpes actually reshapes a person's DNA within only hours of infection, may help address the public health burden of HSV-1.
Globally, nearly 4billion people have this type of herpes and experts are becoming more concerned as drug-resistant strains are developing, which could lead to more transmission.
And unmanaged herpes can lead to devastating complications, traveling to the brain and triggering inflammation, which can increase the risk of dementia.
Researchers in Spain analyzed human cells and infected them with HSV-1, and found almost immediately that it reshapes cell DNA so it can access more genes and spread rapidly throughout the body.
However, blocking the enzyme topoisomerase I, which controls DNA replication, stopped HSV-1 from rearranging genes during infection, stopping it from spreading.
Blocking the enzyme can be done with drugs called topoisomerase inhibitors, which are usually used in chemotherapy regimens to stop DNA from replicating and forming more cancer cells.
This could be the first-ever method of slowing the spread of HSV-1.
The researchers said while more evidence supporting a possible treatment is needed, the study could be the first step in preventing worldwide herpes outbreaks.
Professor Pia Cosma, corresponding study author and researcher at the Centre for Genomic Regulation (CRG) in Barcelona, said: 'In cell culture, inhibiting this enzyme stopped the infection before the virus could make a single new particle.
'That gives us a potential new therapeutic target to stop infection.'
Herpes is most commonly transmitted from a carrier to a person without herpes by touching a cold sore, which actively produces or 'sheds' the virus.
However, it can cause genital herpes by spreading through oral sex.
HSV-1 leads to painful blisters around the lips and mouth, skin and genitals.
When the virus infects a person, it may travel up to a cluster of sensory nerves in the brain and remain dormant there for months or even years after the initial infection.
But in times of stress, severe fatigue, or changes to the immune system, the virus can reactivate, multiply, and travel back to the skin through nerve fibers. These stressful times can result in new blisters in the same area as the initial infection.
The new study, published Thursday in Nature Communications, looked at human A549 cells, which are caused by the cancer lung carcinoma. The cells were then infected with HSV-1 representing one, three and eight hours post infection.
Researchers found after eight hours, HSV-1 had occupied 70 percent of the cells, suggesting it would take less than a day for the virus to completely overtake cell DNA and spread.
Dr Esther Gonzalez Almela, first study author, said: 'HSV-1 is an opportunistic interior designer, reshaping the human genome with great precision and choosing which bits it comes into contact with.
'It's a novel mechanism of manipulation we didn't know the virus had to exploit host resources.'
The researchers then tried to suppress topoisomerase I, which relaxes DNA and makes it easier for it to replicate. They found this 'hindered viral replication.'
The team wrote that suppressing the enzyme stops HSV-1 from progressing, suggesting it could be most beneficial for those in later stages of infection.
Topoisomerase inhibitors are sold under names like etoposide, irinotecan and topotecan to slow the growth of lung, colorectal, ovarian and testicular cancers, among others.
Some are also used to treat multiple sclerosis, a progressive neurological disorder that attacks the spinal cord, by reducing central nervous system inflammation.
They can be given as either pills or intravenously for anywhere from $8 to $61 depending on the method.
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