SARS-CoV-2 also uses neuropilin-1 to infect human cells
Research has shown that, ability of SARS-CoV-2 to infect cells using both ACE2 and neuropilin-1 has made it more infectious than SARS-CoV. An effort to understand the reasons for SARS-CoV-2 infectious rate has led to the discovery of its ability to infect cells using the receptor neuropilin-1.
Quite often, viruses maximise their infectious potential by using multiple factors. High infectivity of SARS-CoV-2 is due to its ability to infect both the upper and lower respiratory system, typically respiratory viruses infect only the lower system. Infecting upper airway cells means the virus is shed when people talk and breathe on top of when they cough or sneeze.
Research has shown that 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. This extra piece binds to neuropilin-1, a human cell surface receptor.
Blocking neuropilin-1 with antibodies, has been shown to significantly reduce infection in laboratory cell cultures. ACE2 is expressed at very low levels in most cells. Factors such as neuropilin-1 make it easier for the virus to infect more easily.
Studies are underway to test the ability of derived molecules to interrupt the connection between the virus and neuropilin.