A new study that researchers conducted in animal models suggests that SARS-CoV-2, the virus that causes COVID-19, may deactivate a pain signaling pathway. This could explain why so many cases of the infection do not cause any symptoms, promoting viral transmission.
Estimates vary widely, but according to the Centers for Disease Control and Prevention’s (CDC) current best estimates, 40% of people with COVID-19 may experience no symptoms.
These people may carry on with their daily activities as usual, without necessarily realizing that they have contracted the virus. This may cause them to spread it unintentionally. For this reason, some scientists refer to people without symptoms as “silent spreaders.”
The CDC also estimate that up to 50% of all SARS-CoV-2 transmission occurs before the onset of symptoms.
One recent study provides a possible explanation for asymptomatic cases and the lack of symptoms early in the course of more serious infections.
SARS-CoV-2 gains entry to its host cells via a receptor in their outer membrane called ACE2. The spike proteins that give the coronavirus its characteristic crown-like appearance latch onto these receptors.
However, the virus can also invade cells when its spikes bind to another membrane receptor called neuropilin.
This receptor’s usual binding partner is called vascular endothelial growth factor A (VEGF-A), which, among other things, promotes the growth of blood vessels.
Crucially, when VEGF-A binds to neuropilin, it also stimulates a pain signaling pathway in the nervous system.
Researchers at the University of Arizona in Tucson have now discovered that the spike protein of SARS-CoV-2 blocks these pain pathways when it locks onto neuropilin.
This suggests that the virus numbs the pain of infection, possibly to the extent that people feel few, if any, symptoms early in the disease.
The findings of this study appear in the journal Pain.Original Source