Okay. I have some background in this and I am trained to read scientific papers so I’ll dissect this paper and dispel some misunderstandings.

SARS-CoV from humans and civets (~99% similarity)

SL-CoV from horseshoe bats

HIV pseudovirus is not the actual infectious HIV-1 strand. It is a derived strand that has the characteristics of HIV but it is not infectious on its own. In this study, it is just a vector to deliver the S protein to the ACE2 receptor.

Pseudovirus definition: “A pseudovirus is a recombinant viral particle with its core/backbone and envelope proteins derived from different viruses1; moreover, the genes inside the pseudovirus are usually altered or modified so that they are unable to produce the surface protein on their own.”

Results:

    Bat SL-CoV S protein cannot bind to human ACE2 so bat SL-CoV cannot enter to infect humans.

    Human SARS-CoV protein cannot bind to bat ACE2 so human SARS-CoV cannot enter to infect bats.

    Switching the receptor regions from SARS-CoV to SL-CoV: the S protein from SL-CoV can enter humans.

    This study was not about the HIV pseudovirus strain. The pseudovirus was injected with the S protein and was used as a delivery method to ACE2 cells. NO ACTUAL ANIMALS WAS USED IT WAS JUST LABORATORY TEST CELLS.

Mechanism of S protein and ACE2: “The two strands show major differences between N-terminal regions in their S proteins.”

S protein is responsible for entry to the host of the virus through binding to a receptor and fusing to the membrane of the host. This means that the S proteins in the two different strands have different mechanisms in binding to the host. The S proteins bind to receptors called ACE2 receptors in humans. There is an identified 193-residue fragment of DNA in the SARS-CoV strand S-protein that is corresponded with this ability to bind to ACE2. They found that mutations (deletions or changes in these 193-residue fragments) could completely stop S protein from binding to ACE2 which would completely stop the binding of the virus.

What they’re trying to test: They found that there is a significant amount of deletion in the S protein from the bat strand. They’re predicting that since there is a huge difference in the bat S protein sequence that they cannot bind the the human ACE2 receptor which means that the SL-CoV will not work in humans.

How they’re testing it:

    HeLa cells: human cell lines used for scientific testing (very widely used) and then it is recreated so that the ACE2 receptors are in the human cell line so that they can test the enzyme activity in these cells. There are human ACE2 with ACE2 with human origins and human cells with ACE2 expressed from bats. NO BATS OR HUMANS WERE INJECTED WITH ANYTHING. THESE ARE ALL CULTURED CELLS.

    Creating recombinant strains: HIV-based pseudovirus are combined with the S protein receptor. Another strand of pseudovirus with a control vector (no S protein). They basically used the S proteins from SL-CoV and SARS-CoV and combined them with the pseudovirus.

    Checking if the strain and ACE2 inhibitors are functional: they did enzyme activity tests (assays) using antibodies obtained from mice to test it. NO ACTUAL MICE WERE USED JUST THEIR ANTIBODIES.

    They perform ACE2 activity tests (assays) to test if the ACE2 and S protein strains worked. They tested the ability of the pseudovirus strains with the different S proteins from different animals to see if it recognizes and binds to human ACE2.