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Herpes simplex virus 1, or HSV-1, is a virus that infects most of the human population. In many people, the virus stays dormant in nerve cells, but in some individuals, it can ‘wake up’ regularly and cause painful facial lesions known as cold sores. In very few cases, the virus can enter the brain and become life threatening.
When HSV-1 encounters a human cell, there are three possible outcomes. The virus can either enter the cell and then replicate uncontrollably, get inside the cell but not multiply, or fail to enter the cell altogether. However, during experiments, researchers do not usually look at individual cells but instead consider whole populations. This makes it hard to understand the exact mechanisms that contribute to a cell resisting or succumbing to the virus.
New approaches are now making it possible to study individual cells over time. Here, Drayman et al. harnessed these methods to understand how individual human cells respond to HSV-1. The experiments show that most cells are actually able to resist the infection. Amongst those, a small fraction managed to stop the virus replicating by initiating a built-in ‘antivirus program’. However, a minority of cells did become highly infected, shutting down the signaling process that fends off the virus. In these cells a different set of genes were switched on, making them more similar to the cells found in embryos. In the process, the virus recruited a protein called β-catenin to help with its multiplication.
There are efforts to develop drugs to interfere with β-catenin, as this protein is also produced differently in people with cancer. Such drugs, if identified and safe in humans, could potentially serve to treat HSV-1 infections.
