Gert
The wording of the question is odd and makes me wonder if the person who said it knows much about the subject. Vaccines cannot become host for anything including mutations. If we assume they meant vaccinated individuals are more likely to generate virulent mutations than those naturally infected then why would/could this happen? The difference between the two lies in the challenge mechanism and here the vaccine technology in question needs to be specified. Some are full spike, some spike RBM only and others whole inactivated. The whole inactivated should create a very similar response to natural infection in that all parts of the packaged virion are capable of priming immune cells what it cannot mimic is the proteins produced in the cell for innate response suppression which are not packaged in the capsid (non-structural and accessory proteins which account for most of the genome) or the relative proportions of the proteins generated by viral mRNA transcription. The other vaccines focus on Spike, or the RBD specifically, and will only generate antibodies to their antigenic sites and T and B cells able to react with peptides from that protein. While these are only a small subset of the antibodies produced in a natural infection they are chosen as the most likely to generate steralising immunity.
How would this effect mutations and virulence? If the antibodies, and immune cells, have been primed to target an important antigenic site (e.g. the receptor binding domain) then random mutations occurring at that point, which would reduce viral binding affinity, would be selected against but if it also stopped antibody binding then it may still be advantageous to the virus, on balance, and increase the variant against the wild type causing vaccine escape. However this has little, if anything, to do with increasing virulence and is just as likely to reduce virulence and make the virus less fit. The virus probably had found a near optimum configuration while the change would only be helpful in the vaccinated with lots of antibodies targeting the specific spike coded for in the vaccine in naive individuals it would probably be out performed. Vaccine generated viral drift was seen in China's influenza poultry population where the genomic distribution of HA made a nice bell curve prior to mass vaccination. Once the vaccine, which targeted the peak of the bell curve, had been in use for a while the Dromedary single hump became a more Bactrian bi-hump with the peak depressed and the two new peaks taking over as the wild type strains. gs can probably supply more of the details but I seem to remember one of the humps went on to be the Fujian strain.
Vibrant asks a couple of questions towards the end of her post.
Making sure everyone, and particularly in high risk groups, are not mineral or vitamin deficient should be standard practice.
As pointed out the first jab produces a response and the second takes that response and greatly increases it. The recommended timing of the booster shot is based on the waning of the effector cell response from the first shot aiming to boost B plasma cell production some of which will, hopefully, become long lived memory B cells ready to mass-produce well targeted IgG on re-challenge. The second dose timing is set as early as possible so maximum immunity can be achieved quickly but the decay curve of the immune response to the first shot is fairly slow and there is normally still plenty to boost if given a month or more later than scheduled, which is the UK reasoning behind delaying the second shot while getting the first dose into more arms. This makes sense as long as the second dose is not delayed too long and you are short of vaccine or staff to administer it.
I looked a little at the prime-boost mechanism from an immunological view in this comment to a question of curiosity’s about giving just one shot.
https://flutrackers.com/forum/forum...-covid-19-new-coronavirus?p=902464#post902464
