The conclusion within the abstract clearly calls for the creation of vaccines for each variant. I'm not sure I saw where they advocate that vaccines cause COVID to be worse.

The first sentence doesn't seem right to me.

There is one and one only reason viruses mutate, and that's from errors during replication. The number of mutation opportunities is identical to the number of replications. A new variant is just a random mutation that enables some kind of competitive advantage versus other variants. So number of replications, mutations, and new variants are all directly related.

How do vaccines make it easier for the virus to replicate?

Debunking the myth that vaccination promotes mutations. Being fully vaccinated actually suppresses them https://t.co/1eD70PpUwr pic.twitter.com/glgiZJ8kXL

— Eric Topol (@EricTopol) August 10, 2021

I know Robert Malone has been discredited to some extent by a lot of other leading global researchers. I take him with a grain of salt simply because he keeps popping up on far right political media outlets and is not debating via more traditional research channels.

The dude does seem imbalanced. Interesting read on him. He is, interestingly, a COVID long hauler who has taken to blaming the vaccine for extending his symptoms.

Atlantic Profile of Robert Malone

Haven't finished reading, but it is interesting.

The N terminal domain (NTD) is part of the spike S1 subunit, and the receptor binding domain (RBD) is what "fits" to the cell. They say the anti-N terminal antibodies are already ineffective, but the virus can mutate a lot in the NTD without screwing up the binding to the receptor.

Since the Pfizer antibodies focus strongly on the receptor binding domain, they say maybe if there's a significant mutation in the receptor binding domain, the Pfizer vaccine will be completely useless. The counterpoint is that the receptor binding domain is like a key for a lock, where the lock is the receptor on the cell. If you mutate there, that may make it less able to bind. So the mutation that would "matter" would be one that makes the antibodies for the receptor binding domain not work as well, but also doesn't prevent binding (or make binding less efficient).

Not so fast my friend, they reply. In addition to ACE2, L-SIGN can also be an entry receptor, and it binds to the N terminal domain, but not the receptor binding domain. So even if the vaccines cover up the receptor binding domain, the N terminal domain is still free to bind. womp womp.

They also propose that this could be a form of antibody enhancement. The wild-type antibodies bind to the N terminal domain but don't neutralize it, which changes the shape of the receptor binding domain, which make it bind better to ACE2. But, they say, this hasn't been observed in humans specifically, but maybe it has in the form of being the explanation for reduced protection.

This is all focused on antibodies, and infections. But it doesn't say anything about cellular immune system response. Something like this could be why infection protection drops, but protection from severe disease doesn't.

It also seems like it would apply also to someone who was originally infected with wild-type and developed antibodies against that.