The concluding paragraph of the originally linked Science paper is revealing: > There is limited knowledge about the virus-host interactions that determine cel

The concluding paragraph of the originally linked Science paper is revealing: > There is limited knowledge about the virus-host interactions that determine cellular entry of SARS-CoV-2. Viruses display considerable redundancy and flexibility because they can exploit weak multivalent interactions to enhance affinity. While the focus to date has been almost entirely on the role of ACE2 in SARS-CoV-2 entry, the expression pattern of ACE2 does not match tissue tropism of SARS-CoV-2. This raises the possibility that co-factors are required to facilitate virus-host cell interactions in cells with low ACE2 expression. NRP1 could represent such an ACE2 potentiating factor; however, it is also possible that SARS-CoV-2 can enter cells independently of ACE2 when viral loads are high. The reason why a number of viruses use NRPs as entry factors could be because of their high expression on epithelia facing the external environment, and their function in enabling cell, vascular, and tissue penetration. NRP1 might explain some of the strange pathophysiology of COVID-19. [1] https://en.wikipedia.org/wiki/Coronavirus_disease_2019#Pathophysiology https://en.wikipedia.org/wiki/Coronavirus_disease_2019#Patho...