A study, published in Science, looked at how SARS-CoV-2 enters cells, and looking at structure of the spike protein and neuropilin-1 on the surface of cells.
Prof Lawrence Young, Professor of Molecular Oncology, Warwick Medical School, said:
“This study provides more insight into the mechanism by which the SARS-CoV-2 virus infects cells. It is a very carefully performed study using cell lines in tissue culture and provides an explanation for why SARS-CoV-2 is more infectious than SARS-CoV. The study demonstrates that neuropilin-1 (NRP1) facilitates the entry of the virus into cells after the virus has initially bound to the ACE2 receptor and that blocking this interaction (either with antibodies or a small molecule inhibitor) can reduce the efficiency of SARS-CoV-2 infection. All these studies are performed in cell lines in culture so there is no information about how NRP1 works in the body and whether blocking this interaction will affect infection. NRP1 has been found to mediate the infection of a number of other viruses (e.g. HTLV-1, EBV) and normally functions in modulating the growth of cells. This means that blocking NRP1 in the body could result in harmful effects.
“I would say this study is another ‘brick in the wall’ of our understanding of the biology of SARS-CoV-2 infection and contributes to an improved understanding of the way the virus infects cells.
“The study will help us as we think about the future of vaccine development and possible anti-viral drugs.
“All the work in this study is in cells in the lab. Studies in pre-clinical models will be the important next step.”
‘Neuropilin-1 is a host factor for SARS-CoV-2 infection’ by James L. Daly et al. was published in Science at 15:00 UK time on Tuesday 20 October 2020.