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Yes, CLL can be a slow progressor. Rituxumab was a breakthrough therapeutic, administered in combination with chemo as R-CHOP. It came on the scene in the early-mid 2000's. There are rituximab biosimilars now. Small molecules, like ibrutinib, also were breakthrough therapeutics.
I was also pre-med back in the day, this thread gives me ptsd. OChem and racist asians helped kill that dream off.
What do you think of the NovaVax alternative? is it safer by any degree?

If the Novavax formulation stays put, that would better than if it becomes a source of soluble spike proteins lookng for cells with ACE 2 receptors to bind to.
The mRNA containing liposome (fat nanoparticle) is taken up, non-specifically, by a cell.
The mRNA is released from the liposome inside the cell where it joins the intracellular protein manufacturing machinery (ribosome) and the spike protein is produced.
Enzymes within the cell chop up the spike protein into peptides that join with Major Histocompatibility Complex (MHC).
The intact protein can also cycle up to the surface of the cell, and in the case of the toxxine coded spike protein, as it is reported to have a transmembrane domain, remain at the surface for a while. It can be released into circulation, or, a piece of cell membrane can enfold around it (endocytosis) and the protein chopped up into peptides within the endosome, where it joins MHC.
The peptide-MHC then cycles to cell's surface.
Peptide-MHC is what the T cell receptor of T cells recognizes, and T cells are alerted to what appears to be a virally infected cell.
CD4 T cells recognize peptide-MHC class II and interact with specific B cells that are turned on to make antibodies to the peptide.
CD8 T cells (killer T cells) recognize peptide-MHC class II and kill the cell displaying it.
Antibodies kill by a few mechanisms. The tail end of the antibody, the Fc (crystallizable fragment) region, attracts Natural Killer (NK) cells whcih have Fc receptors that bind to antibody Fc. The NK cells then kill the cell that has antibody attached to it. Other cell types like macrophage (big eater) cells also have Fc receptors.
The antibody Fc region also triggers complement, a serum protein, to begin a cascading activation series of reactions, that ends with holes being poked into the cell with the antibody attached to it, killing it.
As the spike protein remains at the cell surface, the cell is targeted for destruction by antibodies directed to the spike protein. As the spike protein gets released by the cell into circulation, any cell that it binds to, for example, via the cell's ACE2 receptor, will be targeted for destruction by antibodies. If the spike protein is endoctyosed into this bystander cell, it will be digested, and the peptides displayed on the cell's surface in MHC, targeting it for destruction.
The liposomes are not targeted to any particular type of cell. They bleb into cells nonspecifically. If they were to remain localized at the site of injection, then the T cell-mediated and antibody-mediated damage might remain localized. But if the liposomes were to make their way out of the site of injection, for example, into the circulatory or lymphatic system, then cells that line blood vessels (endothelial cells) could be targeted for destruction. Or if the mRNA liposomes exited capillaries into the surrounding tissue, for example, into the brain or heart, then brain or cardiac cells would be targeted for destruction.
mRNA enclosed in liposomes is a type of transfection reagent, a research tool to study protein expression in celll lines. mRNA can also be coded to knock out protein expression, a useful application. But injecting humans with non-targeted transfection reagents is extremely risky, and while being applied as a cancer therapy, it may be worth the risk, and only in controlled clinical studies with patient consent and institutional review board authorization. But being used in healthy persons to mitigate a low-probability mortality risk is very unwise and should be a crime.