The usual group of media misinformation/hate-peddlers (Tucker Carlson), Christian influencers/hate-peddlers (Allie Beth Stuckey), and misinformation-for-profit-peddlers (Peter McCullough, Stew Peters, Steven Kirsch, Robert Malone, etc) and politicians (Marco Rubio, Marjorie Taylor Greene, and others) are using their influence to peddle absolute nonsense about genetically modified organisms.
The latest round of accusations and insinuations is that Pfizer is performing "gain of function" research on SARS-CoV-2 in order to sell more vaccines or more antivirals. This is, of course, complete and utter bullshit.
Virtually all modern genetic research involves modifying the genomes of living organisms or viruses. In Pfizer's case, that comes down to a couple specific situations.
Case 1: There are virus-specific mechanisms that have been developed in order to have cell-lines (like Vero E6) express the protiens of specific viruses so they can be studied. When a new "variant of concern" is identified, the gene that codes for the S protein of that new variant is inserted into one of the ancestral SARS-CoV-2 genomes (replacing the existing spike-encoding gene) in order to create sufficient quantities of that protein for study. This is a common approach to studying viral proteins, and has been done many times and in many labs. There is no "functionality" being gained by this chimeric virus. It exists only to enable the expression of the S protein for study and for vaccine design.
Case 2: This is a little more complex to explain, but stay with me for the biology lesson: When SARS-CoV-2 enters the cell, it relies on the ribosomes in that cell to translate its RNA into proteins. The output of that translation process isn't individual proteins... instead the expressed product is a few small enzymes (such as proteases) and a pair of large polyproteins that are composed of the viral proteins that are necessary for replication. Those polyproteins are non-functional, and cannot be incorporated into new virions until the individual proteins are cleaved apart. The enzymes that do that cleaving are called proteases. Any given protease is typically very specific about the cleavage sites that it can bind to (and therefore cleave). There is a class of drugs called protease inhibitors (Pfizer's "Paxlovid" is an example) that are small molecules that can bind to those specific cleavage sites on the polyproteins. With those cleavage sites blocked by the protease-inhibitor molecules, the viral proteases can't cleave the polyprotein into functional units, and new infectious virions can't be created.
It's important to realizes that those cleavage sites have nothing to do with the viruses ability to bind to or infect a cell. They are only related to how the virus assembles new copies of itself after the virus has already gained entrance to the cell's cytoplasm. The genes that control the specific shape of those cleavage sites are subject to natural mutation. In order for companies that produce protease-inhibitors to predict their function in the field (in which mutations naturally occur all the time), it's important to (in vitro, in a lab) create conditions under which those cleavage sites mutate. In order for protease inhibitors to remain useful in the battle against disease, virologists absolutely must be able to prove that those inhibitor molecules can bind-and-block to all likely mutations of the cleavage site. There is no "functionality" gained by allowing these cleavage-site mutations to occur in a controlled setting. The virus does not become more transmissible, nor more deadly.
For the four or five of you that read this far, thanks.