Half of the Americans suffer from an incurable disease that causes painful – and embarrassing – blisters and ulcers around the mouth.
About 122 million people have Herpes Simplex Virus 1 (HSV-1), the oral tribe of Herpes. It is scattered, through dense skin to skin contact and differs from the sexually transmitted herpes simplex virus 2 (HSV-2), which causes genital blisters and ulcers.
There is no remedy for HSV-1, but antiviral medicines can manage outbreaks and reduce the risk of transmission.
Now, however, researchers from Spain have discovered how the virus works on a person’s DNA and the door opens for a possible remedy.
The team discovered that the virus ‘Kaaft’ a certain enzyme in the body with which Herpes can replicate itself, but if that enzyme is blocked, it brings the hostile acquisition to a standstill. “
The researchers are hopeful that the findings of the study, which offer the first proof of herpes, can actually help the DNA of a person within just a few hours after infection, to tackle the public health burden of HSV-1.
Almost 4 billion people worldwide have this kind of herpes and experts are more concerned as drug -resistant tribes develop, which can lead to more transfer.
And unmanned herpes can lead to devastating complications, traveling to the brain and activating inflammation, which can increase the risk of dementia.
Research published this week in Nature Communications showed that medicines that are usually used in the treatment of cancer can prevent the herpes virus from spreading in the body (stock image)
Researchers in Spain analyzed human cells and infected them with HSV-1, and found Almost immediately the cell -DNA reforms so that it has access to more genes and quickly spreads over the body.
However, blocking the enzyme Topoisomerase I, which controls DNA replication, stopped that HSV-1 rearranges genes during the infection, so that it cannot spread.
Blocking the enzyme can be done with drugs called topoisomerase inhibitors, which are usually used in chemotherapygimes to prevent DNA from replicating and forming more cancer cells.
This can be the very first method to delay the spread of HSV-1.
The researchers said that although more evidence is needed to support a possible treatment, the study could be the first step to prevent global herpes outbreaks.
Professor Pia Cosma, corresponding study author and researcher at the Center for Genomic Regulation (CRG) in Barcelona, said: ‘In cell culture, the braking of this enzyme stopped the infection before the virus could make a single new particle.
“That gives us a potentially new therapeutic target to stop infection.”
Herpes is usually transferred from a carrier to a person without herpes by touching a cold pain, who actively produces or throws the virus.
However, it can cause genital herpes by spreading oral sex.
HSV-1 leads to painful blisters around the lips and mouth, skin and genitals.
When the virus infects a person, traveling to a cluster of sensory nerves in the brain and sleeping there for months or even years after the first infection.
But in times of stress, severe fatigue or changes in the immune system, the virus can re -activate, multiply and travel back to the skin by nerve fibers. These stressful times can lead to new blisters in the same area as the initial infection.
The new study, published on Thursday in Nature communicationLooked at human A549 cells, which are caused by cancer lung carcinoma. The cells were then infected with HSV-1 that represent one, three and eight hours after infection.
HSV-1 causes painful blisters, cooling swears, around the mouth and lips. Although antiviral drugs can treat symptoms, there is no remedy for the virus itself (stock image)
The graph above shows the global prevalence of herpes. HSV-1 is oral Herpes and HSV-2 is genital herpes
Researchers discovered after eight hours, HSV-1 had occupied 70 percent of the cells, which suggests that it would take less than a day before the virus would fully overtake cell DNA and spread.
Dr. Esther Gonzalez Almela, first study author, said: ‘HSV-1 is an opportunistic interior designer, who reforms the human genome with great precision and choosing which bits it comes into contact with.
“It is a new manipulation mechanism that we did not know the virus had to exploit host sources.”
The researchers then tried to suppress Topoisomerase I, which relaxes DNA and makes it easier to replicate. They found this ‘hindered viral replication’.
The team wrote that suppressing the enzyme HSV-1 prevents it from progressing, which suggests that it could be the most beneficial for people in later stages of infection.
Topoisomerase inhibitors are sold under names such as Etoposide, Irinotecan and Topotecan to delay the growth of lung, colorectal, ovary and testicular cancers, among other things.
Some are also used to treat multiple sclerosis, a progressive neurological disorder that attacks the spinal cord by reducing inflammation of the central nervous system.
They can be given as pills or intravenous for everywhere from $ 8 to $ 61, depending on the method.
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