Actually letting the virus mutate without adequate immune response is what produces those variants, as you remove local minima from the evolutionary chain. The

Actually letting the virus mutate without adequate immune response is what produces those variants, as you remove local minima from the evolutionary chain. The fact that most VOCs popped in areas with little to no vaccination coverage quite aligns with that. For omicron the main hypothesis is it actually evolved in a severely immunocompromised HIV patient. Edit: This isn't exactly new[0] and it's also been witnessed for SARS-CoV-2[1]: > These compilations of case reports indicate the need to identify whether certain forms of immunosuppression are associated with an increased risk of such multimutational escape patterns — for instance, specific cancers or specific therapies, such as the development of B-cell aplasia related to CAR T-cell or anti-CD20 therapy, prolonged use of glucocorticoids, long-term chemotherapy, or radiotherapy. Similarly, organ transplant recipients and those with untreated or poorly controlled human immunodeficiency virus infection may also have prolonged SARS-CoV-2 infection and could constitute a reservoir of divergent escape variants that can spread in the general community. Prolonged viral replication in the context of an inadequate immune response facilitates the emergence of immune-pressure escape mutations.[0] I'd appreciate an actual counter argument, other than a poorly understood Marek disease analogy. [0]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4249157/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4249157/ [1]https://www.nejm.org/doi/full/10.1056/NEJMsb2104756 https://www.nejm.org/doi/full/10.1056/NEJMsb2104756