Chickenpox and herpes are caused by viruses from the alphaherpesvirus subfamily. These viruses can cause two types of infection: active, which involves a variety of cells, or inactive, which involves hiding in the peripheral nervous system (PNS). Inactive infections are not necessarily inactive forever; when infected cells sense stressful events the viruses can come out of hiding. Antiviral drugs treat and prevent active, but not inactive, infection.
The PNS is made up of nerve cells called neurons, which pass messages, as electrical 
signals, throughout the body. For the purpose of this summary, a neuron can be divided into three parts. There are dendrites, which bring electrical signals to the cell body, there is the cell body, which makes proteins to support the neuron, and there are axons, which take information away from the cell body to other cells. Axons are very skinny, but can be up to 1 meter in length, which allows herpesviruses to traverse great distances in the body.
Long-term inactive infection allows herpesviruses to persistently infect an individual for life. However, researchers have struggled for decades to develop models to study inactive infection, and the all-important stress-induced transition to active infection. Previously, researchers found that physically separating axons from cell bodies using chambers forced herpesviruses to establish an inactive infection. In this article by Koyuncu et al., the researchers studied the signals that stimulate inactive viruses to reactivate. They identified two ways that viruses ‘wake up’ from inactive infection: the slow way mediated by cellular stress signals, and the fast way mediated by viral proteins.
This work by Koyuncu et al. contributes to the growing overall understanding of herpesvirus infections. The next logical step will be to determine whether reactivation in this model system allow production of infectious viruses.
Summary written by: Serena Drouillard
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