Researchers at Harvard Medical School are discovering more and more about herpesviruses latency periods that give us insight into how the infection is able to be sustained in the cells, waiting and “ready to strike.” The research team, which included Microbiology and Genetics Professor David Knipe, found that the herpes simplex viruses use a “host protein called CTCF, or cellular CCCTC-binding factor” in order to control its own latency and active cycles. CTCF protein is able to bind to viral DNA and act as a key regulator. This host protein and viral interaction is an incredible advantage for the herpes simplex viruses as it allows the virus to go from silent to active meaning that the pathogen can continue on from one host to the next. During the latent period of herpesvirus infection, there are no symptoms and the virus does not replicate due to latency genes (LAT) turning off the genes that encode for viral RNA transcription. Next to the LAT gene is a gene called the ICP0 that stimulates replication and indicates active viral infection. The alteration of these two genes along with the new finding that the CTCF protein enhances this alteration is important in learning more about persistence in herpesvirus. In a knockout gene mice study, the researchers found that without the CTCF binding sites, the protein had nowhere to bind to and thus hindered the herpesvirus’ ability to switch from silent to active infection.
-Meley
https://medicalxpress.com/news/2018-03-infection-herpes-lurks-nerve-cells.html
-Meley
https://medicalxpress.com/news/2018-03-infection-herpes-lurks-nerve-cells.html
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