Figure: Photo Source: Centers for Disease Control and Prevention Public Health Image Library

New research from two separate papers shows that SARS-CoV-2, the virus that causes COVID-19, uses a receptor called neuropilin-1 to efficiently infect human cells. Neuropilin-1 is very abundant in many human tissues including the respiratory tract, blood vessels, and neurons.

Unlike other respiratory viruses, SARS-CoV-2 also infects the upper respiratory system including the nasal mucosa, and consequently spreads rapidly. The starting point for the group of Giuseppe Balistreri at the University of Helsinki involved in the first study was, why did SARS-CoV-2 spread in such a different way than SARS-CoV even if they use the same main receptor ACE2?

To understand how these differences can be explained, the researchers looked at the viral surface proteins, the spikes that like hooks, anchor the virus to the cells. Giuseppe Balistreri's group at the University of Helsinki reveals that when the SARS-CoV-2 genome sequence became available, they were surprised to see that compared to its older relative, the new coronavirus had acquired an ‘extra piece' on its surface proteins, which is also found in the spikes of many devastating human viruses, including Ebola, HIV, and highly pathogenic strains of avian influenza, among others.

They found that neuropilin-1, known to bind furin-cleaved substrates significantly increases the infectivity of SARS-CoV-2. Pathological analysis of human COVID-19 autopsies revealed SARS-CoV-2 infected cells positive for neuropilin-1. The group established that the Spike protein of SARS-CoV-2 does indeed bind to neuropilin-1. The researchers were able to significantly reduce infection in laboratory cell cultures by specifically blocking neuropilin-1 with antibodies. Balistreri said, "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."

For more details, read the article in Genetic Engineering & Biotechnology News.