I think that the ACE-2 enzyme plays the major role in the COVID-19 pathogenesis as it counteracts the ACE enzyme and when the SARS-CoV-2 downregulates the ACE-2 enzyme, angiotensinogen-II is not converted to angiotensin and thus there is activation of the pro-inflammatory and fibrotic as well as inflammatory pathways leading to increased tissue damage. The SARS-CoV-2 virus primarily attacks the main functional receptor i.e. ACE-2 and exerts its inflammatory properties.

Check out the BioRxiv paper from Singh et al 2020, titled “A singke cell Rnaseq expression map of human coronavirus entry factors.” This paper summarizes the SCARFS that control SARS-CoV2 entry.

1. ACE2 is a SARS-CoV-2 receptor that may affect the antiviral immune response

2. Dipeptidyl peptidase 4 is a coronavirus receptor, which may also be associated with the antiviral immune response

3. The SARS-CoV-2 spike-host cell receptor GRP78 binding site

for more useful information :

Article Targeting SARS-CoV-2 Receptors as a Means for Reducing Infec...

ACE2

ACE2 is the main receptor for the SARS-CoV-2 virus.

https://jvi.asm.org/content/94/7/e00127-20

ACE2

Agree with Dr. Sadanand Pandey

ACE2 serves as a primary receptor for the SARS‐CoV‐2 spike protein (S protein) to bind and enter human cells. The receptor‐binding domain of the virus S protein binds to ACE2 causes SARS‐CoV‐2 to undergo endocytosis and exposes it to endosomal proteases leading to viral infection in the host. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7883063/

Check https://pubmed.ncbi.nlm.nih.gov/33368788/

RBD that specifically recognizes ACE2 as its receptor

Also have a look at this:

Article Phosphatidylserine receptors enhance SARS-CoV-2 infection