ACE2 Receptor Expression
Undifferentiated cells expressing little ACE2 were poorly infected with SARS-CoV, while well-differentiated cells expressing more ACE2 were readily infected. Expression of ACE2 in poorly differentiated epithelia facilitated SARS spike (S) protein-pseudotyped virus entry. Consistent with the expression pattern of ACE2, the entry of SARS-CoV or a lentivirus pseudotyped with SARS-CoV S protein in differentiated epithelia was more efficient when applied to the apical surface. Furthermore, SARS-CoV replicated in polarized epithelia and preferentially exited via the apical surface. The results indicate that infection of human airway epithelia by SARS coronavirus correlates with the state of cell differentiation and ACE2 expression and localization. These findings have implications for understanding disease pathogenesis associated with SARS-CoV and NL63 infections.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287568/
Description of mechanism of HCQ
https://www.nature.com/articles/s41421-020-0156-0
https://chemrxiv.org/articles/Energetics_Based_Modeling_of_Hydroxychloroquine_and_Azithromycin_Binding_to_the_SARS-CoV-2_Spike_S_Protein_-_ACE2_Complex/12015792
And apparently, they've been studying the effects of HCQ on coronaviruses for quite some time… this published in 2005…
https://virologyj.biomedcentral.com/articles/10.1186/1743-422X-2-69