2600 bro wrote:
Again, you are wrong. Robust, broad Tcell immunity is key for minimizing symptoms and quick clearance of the virus post-infection. The problem is if one does not develop broad Tcell immunity when you're young and healthy you will not have it later in life when you need it. Natural infection produces T-Cell immunity against the entire virus including the envelope protein, the Nucleocapsid protein, the replicase protein etc. Further, it is becoming clear that this virus not only binds and infects via the spike protein but also does so passively via cell-cell projections causing cellular fusion and production of multinucleated cells. The latter mode of transmission is resistant to IgG Ab/vaccines. No surprise the Indian Delta variant has evolved to demonstrate enhanced cell-cell transmission- aka is more resistant to the vaccines (surprise!! Variants evolving to evade targeted spike-directed vaccines and therapeutics). So this shows your in vitro IgG neutralization assays, really, at the end of the day are a very poor clinical correlates of protection. Your siloed understanding of this virus is underwhelming. Stop internalizing all the information that has been spoon fed to you and open your eyes.
No comment on Manaus yet.... telling :)
No vaccines are completely protective, they never will be. Even 75% effectivity (see: Delta variant) makes widespread transmission difficult.
If your threshold is complete protection then NOTHING will ever satisfy you.
Infection driven immunity falls on a wide spectrum. You cannot ensure a strong response, ad it's hard to test for adequate response from prior infection. Allowing mass infections is going to provide orders of magnitudes more replication events, variation, and selection (another fact you refuse to acknowledge) - and carries enormous cost to a population...
Yes it's possible that other viral epitopes are useful for driving immune response but the spike is by far the most antigenic and potent. The most important epitopes for immunity overlap with the important regions for receptor binding... making selection for increased potency but decreased neutralization very difficult.
You are taking all the exceptions and edge cases and making them the focus. There are many more exceptions and edge cases to infection driven immunity.
You do seem to have read some fringe blogs and can spam buzzwords though. One of the better trolls around here.
Manaus never reached herd immunity. Natural immunity produces broad, robust and long term memory B cell immunity to many viral epitopes. The envelope protein, Nucleocapsid protein, RdRP all play a role in dampening innate host cell response, disrupting normal cell processes and spreading infection. The simple spike-bind-ACE2R mode of infection is only one of the many means by which SARSCoV2 infects and spreads throughout the body (neutrophilin1, CD147, Syncytial spread). It is probable that the envelope and membrane proteins also play roles in docking/infection. The data show that vaccines, while reasonable choices to minimize risk for people who are at risk, certainly are not superior and may in fact be inferior to natural immunity. Clinging to your dogmatic but false/unstudied beliefs is just foolish.