Scientists have unlocked a key reason why the novel coronavirus is so infectious, identifying an extra receptor that facilitates the virus’s entry into cells that may also explain why COVID-19 causes neurological symptoms.
When the SARS-CoV-2 virus first emerged in Wuhan, scientists quickly learned that the virus enters the body’s cells when its distinctive spike protein binds to a receptor known as ACE2.
Now scientists from the University of Helsinki, the Technical University of Munich and the University of Queensland, working in collaboration, have identified that SARS-CoV-2 can also enter cells using another receptor, called neuropilin (NRP1).
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The scientists published their findings in the journal Science.
Another study conducted by scientists from the University of Bristol and published in the same edition of the journal reported that the binding between NRP1 and the coronavirus’s spike protein could be disrupted by a small molecule antibody, reducing the virus’s infectivity.
Giuseppe Balistreri from the University of Helsinki said antibodies that blocked NRP1 were able to block SARS-CoV-2 infection by 40 per cent, indicating that the receptor played a key role in the virus’s infectivity.
Dr Balistreri said the virus’s sequence has an “extra piece” that was not seen in the SARS virus from 2002-03 but has also been observed in other viruses, including HIV, Ebola, Zika virus and avian influenza.
“They all have this little code on their surface,” Dr Balistreri said. “It is exactly this extra part that binds to the neuropilin.
“Basically, when the virus has this extra piece, it becomes 10 times more powerful, particularly in human cells.
“Therefore a more general idea is being investigated in our labs that perhaps every virus has its main door, but if they have this extra little piece, they can access a much wider lock, which is neuropilin, and this could give access to broader spreading.”
The fact SARS did not have the “extra piece” on its sequence that binds to neuropilin explains why it was nowhere near as infectious as SARS-CoV-2, and the SARS epidemic was contained within a year with fewer than 9000 cases reported.
Frederic Meunier, a professor in UQ’s Queensland Brain Institute, said neuropilin was present not only in the upper respiratory tract but also in brain cells.
Dr Balistreri and his colleagues are now developing prototype molecules that they hope could block access to the tissues targeted by SARS-CoV-2 that cause disease.
Health Editor
Sydney
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2020-10-21 10:30:00Z
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