For the first time, American researchers have identified a new mechanism that explains why the herpes virus alternates between dormant and active stages.
Caused by the Herpes Simplex Virus (HSV), herpes is a common infectious disease that can affect different parts of the body, starting with the lips and genitals and, in the most severe cases, the eyes. In France, it is estimated that 10 million people are affected by herpes labialis, 2 million by genital herpes, and 60,000 by ocular herpes.
If it is possible to control the effects of herpes, in particular thanks to antiviral creams, our body never gets rid of the virus. The latter alternates between sleep phases in nerve cells and outbreaks, during which it is particularly virulent.
But how to explain this alternation between “latent” stage and “lytic” stage where the herpes virus is active? Researchers at Cornell University in the United States have found the answer. In study published in the journal PLOS Pathogensthey explain that the virus goes from one stage to another depending on the degree of concentration of its DNA in the structure called chromatin.
“Any problem caused by herpes is due to the reactivation of latency,” explains Dr. Luis Schang, of the Baker Institute for Animal Health. This is why antivirals cannot cure the infection and why, until now, it has been impossible to develop a vaccine. Latency and reactivation are central to herpes virus research.”
Hope for a cure or a vaccine
To understand how herpes alternates dormant and active phases, we must look at the very nature of the HSV virus. When it enters a cell, the cell tries to protect itself by wrapping the viral DNA tightly around coil-shaped proteins called histones and condensing it into chromatin, which causes the virus to become dormant. But if cells fail to block viral DNA, chromatin no longer plays its role. She then lets the virus particles activate their genes and replicate using the cell’s machinery to trigger a lytic infection, causing a flare-up.
So far, the majority of studies have focused on when and how individual genes in the herpes virus genome are turned on and off during infection to understand how the virus transitions from latent to lytic stage.
In this new work, the researchers show that chromatin dynamics regulates whether the entire herpes virus genome is activated, which must occur before individual virus genes are expressed.
The discovery of this new mechanism is important because it opens the way to a new way of exploring the interaction between the herpes virus and host cells. By determining whether viral DNA is expressed or not, scientists hope to be able to develop an effective antiviral treatment or a vaccine against herpes, which has not been possible so far.
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