A study by the University of Helsinki, carried out in the frame of the Long COVID project, has discovered the main mechanism of SARC-CoV-2 neuronal infection using a human iPSC-derived neural cell model. The productive infection was ACE2 dependent and TMPRSS2 independent. The study also found that the virus used the late endosomal and lysosomal pathway for cell entry and that the infection could be blocked by inhibitors of host phosphoinositol-5 kinase.
The relevant findings of this study led by Giuseppe Balistreri has been published in the Journal of Virology.
The first Long COVID project peer-reviewed article can be found below:
SARS-CoV-2 Infection of Human Neurons Is TMPRSS2 Independent, Requires Endosomal Cell Entry, and Can Be Blocked by Inhibitors of Host Phosphoinositol-5 Kinase | Journal of Virology (asm.org)