Imagine being infected with a deadly virus that makes you impervious to pain. By the time you realize you are infected, it’s already too late. You have spread it far and wide. Recent findings in my lab suggest that this scenario may be one reason that people infected with SARS-CoV-2, the virus causing COVID-19, may be spreading the disease without knowing it.
Most accounts to date have focused on how the virus invades cells via the ACE2 protein on the surface of many cells. But recent studies, which have not yet been peer-reviewed, suggest there is another route to infecting the cell that enables it to infect the nervous system. This led my research group to uncover a link between a particular cellular protein and pain – an interaction that is disrupted by the coronavirus. Our research has now been peer-reviewed and will be published in the journal PAIN.
I am a scientist who studies how proteins on cells trigger pain signals that are transmitted through the body to the brain. When these proteins are active, the nerve cells are talking to each other. This conversation occurs at deafening levels in chronic pain. So by studying what causes the excitability of nerve cells to change, we can begin to unravel how chronic pain becomes established. This also allows us to design ways to mute this conversation to blunt or stop chronic pain.