Are there people in our population, resistant to coronavirus?

Continue to study the question of coronavirus and what can be done about the bioinformatics connections associated with this I found an article on the fact that in lung cells the virus attaches to the ACE2 protein.
All viruses must multiply, and each virus needs to penetrate the host cell and the first stage on this path is to connection to the cell surface. In case of coronavoirus this is the ACE2 protein, which is encoded by the gene of the same name.

The penetration of viruses into the cell from https://www.ncbi.nlm.nih.gov/pubmed/10811925

ACE2: https://www.proteinatlas.org/ENSG00000130234-ACE2/tissue

Compared to the small intestine — in the lungs, very ACE2 is in very small percentage cells. We have the opportunity to observe individual cells — let’s look at the cells of the lungs and intestines, which have ACE2 type in their cells. PanglaoDB: to answer this question

In the picture we see 11 thousand cells from the human lungs, which are divided into clusters depending on the types of cells — the lungs consist of many cells of various types https://panglaodb.se/view_interactive_tsne_data.html?sra=SRA640325&srs=SRS2769051&plot=umap&overlay=ACE2

it can be seen that there is really little gene product, and it is found only in type 2 fibroblasts and alveolar cells (whatever that means)

Now, let’s go back a bit to viruses and how they cling to our cells. Scientists have studied the human immunodeficiency virus, which attaches to the CCR5 receptor on human cells. There is even a 3D model obtained by x-ray diffraction analysis — how HIV attaches to CCR5:

The red protein below is the human CCR5 receptor, one of the HIV proteins has attached itself to it http://www.rcsb.org/3d-view/6MET/1

Zoom directly to the attachment point

and so it turned out that there is a certain percentage of people who genetically carry a slightly different version of the CCR5 gene — they have a 32 nucleotide deletion that does not really interfere with a person’s life, but prevents the HIV virus from attaching to the cells of such a person, making it in some sense more resistant to the virus. This mutation has a catchy name — rs333

https://www.ncbi.nlm.nih.gov/snp/rs333#clinical_significance

Frequencies in different populations according to gnomAD https://gnomad.broadinstitute.org/variant/3-46414943-TACAGTCAGTATCAATTCTGGAAGAATTTCCAG-T?dataset=gnomad_r2_1

having all these databases on hand is easy to see if there is anything similar for the ACE2 gene — respectively — whether there are at least potentially people who are resistant to coronavirus. At least we have all the information — firstly, there are the results of an X-ray diffraction analysis of the attachment of coronavirus to ACE2, let’s look at them

This time, the red coronavirus particle that clings to ACE2 http://www.rcsb.org/3d-view/6ACG/1

we see that coronavirus attaches to ACE2 in the region of 488th amino acid

Now we open the ACE2 gene in the database of gnomAD genetic polymorphisms, in which we previously looked at the frequencies of mutations in HIV resistance:

https://gnomad.broadinstitute.org/gene/ENSG00000130234?dataset=gnomad_r2_1

Now we look at what is interesting for mutations in the region of 450–500th amino acids:

we see that nature hasn’t created anything outstanding in this place, but for comparison we’ll look at CCR5 — the region of the 180th amino acid:

My prediction is that since it’s very popular to edit genomes right now, most likely in some laboratory they will make a version of ACE2 that, while remaining functionally active, will be invisible to coronavirus.

We will see if this forecast comes true and thanks for your attention!