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“If you think of ACE2 as a door lock to enter the cell, then neuropilin-1 could be a factor that directs the virus to the door,” says Balistreri.
Given the density of neuropilin-1 along nerve tissues in the human nasal cavity, it essentially acts as a welcoming party for SARS-CoV-2 which then only needs to flash its ACE2 before it can engage in a free-for-all inside the human body, with destructive consequences witnessed the world over.
Experiments on mice confirmed the receptor’s role in the virus gaining access to their nervous system, though a direct link to the traumatic damage witnessed on human brains after severe Covid-19 has yet to be properly studied.
“We could determine that neuropilin-1, at least under the conditions of our experiments, promotes transport into the brain, but we cannot make any conclusion whether this is also true for SARS-CoV-2,” says neurologist Mika Simons from the Technical University of Munich.
The researchers have begun exploring ways to interrupt the connection between the virus and neuropilin-1, with a view to making it less infectious, with promising early results and laboratory tests already underway.
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