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Discovery reveals mechanism that turns on and off herpes virus



  Herpes
Credit: CC0 Public Domain

New research by Dr. med. Luis M. Schang and his group at the Baker Institute for Animal Health have identified a new mechanism that plays a role in controlling how the herpesvirus switches between resting and active stages of infection.

The herpes virus causes cold sores and genital wounds as well as life-threatening infections in neonates, encephalitis and corneal blindness.

Treating the virus is difficult as it hides in nerve cells and develops months or years later to reactivate the infection.

In Gang's group, Mi Yao Hu and Esteban Flores Cortes discovered that the virus switches between the "latent" stage and the "lytic" stage, in which it actively replicates, depending on how tight it is. DNA is bundled packaged as chromatin.

Their findings are contained in a publication "Chromatin Dynamics and the Transcriptional Competency of HSV-1

Genomes in Lytic Infections," published November 14 in PLOS Pathogens . Schang's group collaborated with scientists from the University of Alberta, Canada, and University College London (UCL).

"Any problem that causes herpes is due to reactivation due to latency," said Schang. "That's why antiviral drugs can not cure the infection and why it's been impossible to develop a vaccine, and latency and reactivation play an important role in herpes virus research."

When the herpes virus invades a cell, the cell tries to protect itself by wrapping the viral DNA tightly around coil-like proteins, called histones, and condensing it into chromatin, causing the virus to go to sleep. However, if the cells are unsuccessful, the chromatin is only loosely bundled, leaving the viral DNA accessible. The virus particles can then turn on their genes and replicate using the cell machinery to trigger a lytic infection that causes disease.

Most researchers have focused on when and how individual genes of the herpesvirus genome turn on and off during infection. Find out how the virus switches between latent and lytic stages. In the new study, however, the group showed that the dynamics of chromatin regulates whether the entire herpesvirus genome is activated. This must be done before individual genes can be expressed. This new mechanism represents a previously unknown way to regulate gene expression at the level of the entire viral chromosome.

With this new knowledge, researchers can study the interaction between virus and host cells, which determines the expression of viral DNA. Antiviral drugs for the treatment of herpes have been around since the 1960s, but so far, a cure or effective vaccine has not been within reach.

"Latency and gene regulation are a big problem because we do not know nearly enough about it," he said. "It's a big black box in herpes biology."

The discovery opens new avenues for investigating how the virus reactivates when inactive. The ability of herpes to calm down has thwarted efforts to develop effective vaccines or antiviral drugs that completely prevent or cure the infection.


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Further information:
MiYao Hu et al., Chromatin Dynamics and the Transcriptional Competency of HSV-1 Genomes in Lytic Infections, PLOS Pathogens (2019). DOI: 10.1371 / journal.ppat.1008076

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Discovery reveals mechanism for turning on and off the herpes virus (2019, November 14)
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