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Thursday, 21 November 2019

Discovery reveals mechanism that activates and deactivates herpes virus

Researchers at the Baker Institute for Animal Health have discovered a mechanism that plays an important role in controlling the alternation of the herpes virus. He would be involved in the switch between dormant and active stage of the virus.

The herpes virus is formidable and especially very embarrassing for people with the disease. It can cause "cold sores" and genital lesions, as well as life-threatening infections in newborns, encephalitis and corneal blindness. The treatment of the virus is difficult because it hides in the nerve cells and emerges months or years later to reactivate the infection.

Led by Dr. Luis M. Schang, Mi Yao Hu and Esteban Flores Cortes, a research team at the Baker Institute for Animal Health in New York, discovered that the virus is changing from "latent" to "lytic" ( in which it replicates actively) depending on the narrowness of the structure within which the DNA is packaged, chromatin. The results of the study were published on November 14 in the journal PLOS Pathogens .

Schang's group collaborated with scientists at the University of Alberta, Canada, and University College London (UCL).

" Any problem that herpes causes is due to the reactivation of latency,  " said Schang. " That's why antivirals can not cure the infection and why so far it has not been possible to develop a vaccine. Latency and reactivation are major axes of research on the herpes virus.

Histones, proteins around which DNA wraps

When the herpes virus enters a cell, it attempts to protect itself by tightly wrapping the viral DNA around the histones (coil-shaped proteins) and condensing it into the chromatin, resulting in dormancy. of the virus. But if the cells fail in this process, the chromatin is only weakly bound, leaving the viral DNA accessible. The virus particles can then activate their genes and replicate using the cellular machinery to trigger a lytic infection, causing the disease.

Most researchers focused on the timing and process of activation and deactivation of individual genomes of the herpes virus genome during infection, to determine how the virus switches between latent and lytic stages.

Diagram (from another study ) explaining how stress stimulates the reactivation of HSV at the "latent" stage. A pathway of neuronal stress involving the activation of the c-Jun N-terminal kinases (JNK) is crucial for the reactivation of the virus. JNK signaling induces histone phosphorylation of viral promoters, thus linking cell stress to viral gene expression. Credits: Cliffe et al.

A hitherto neglected way of regulating the expression of the genes of the virus

In the new study, however, the group showed that chromatin dynamics regulates genome activation of the herpes virus as a whole, which must occur before each gene can be expressed. This new mechanism represents a hitherto neglected way of regulating the expression of genes at the level of the whole of the viral chromosome.

With this new knowledge , researchers can further explore the interaction between virus and host cells determining whether viral DNA is expressed or not. Antiviral drugs to treat herpes have been around since the 1960s, but so far no cure or effective vaccine has been possible.

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

The discovery opens new perspectives to explore the reactivation of the virus after a period of latency. The ability of herpes to hide has hitherto thwarted efforts to develop effective vaccines or antiviral drugs to prevent or completely cure the infection.


Article: Chromatin dynamics and the transcriptional competence of HSV-1 genomes during lytic infections

Authors: MiYao Hu, Daniel P. Depledge, Esteban Flores Cortes, Judith Breuer, Luis M. Schang

PLoS Pathog 15(11): e1008076.

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