Excerpts from [1]:
- "The spike protein receptor-binding domain (RBD) of SARS-CoV-2 is the molecular target for many vaccines and antibody-based prophylactics aimed at bringing COVID-19 under control."
- "Such a narrow molecular focus raises the specter of viral immune evasion as a potential failure mode for these biomedical interventions. With the emergence of new strains of SARS-CoV-2 with altered transmissibility and immune evasion potential, a critical question is this: how easily can the virus escape neutralizing antibodies (nAbs) targeting the spike RBD?"
- "Our modeling suggests that SARS-CoV-2 mutants with one or two mildly deleterious mutations are expected to exist in high numbers due to neutral genetic variation, and consequently resistance to vaccines or other prophylactics that rely on one or two antibodies for protection can develop quickly -and repeatedly- under positive selection."
- "The speed at which nAb resistance develops in the population increases substantially as the number of infected individuals increases, suggesting that complementary strategies to prevent SARS-CoV-2 transmission that exert specific pressure on other proteins (e.g., antiviral prophylactics) or that do not exert a specific selective pressure on the virus (e.g., high-efficiency air filtration, masking, ultraviolet air purification) are key to reducing the risk of immune escape"
- "Strategies for viral elimination should therefore be diversified across molecular targets and therapeutic modalities"
[1] Risk of rapid evolutionary escape from biomedical interventions targeting SARS-CoV-2 spike protein (April 2021) https://pubmed.ncbi.nlm.nih.gov/33909660/
And yet, the Delta variant evolved in an 100% unvaccinated population - and is quite happily punching through some of the protections afforded by vaccines, despite not having any evolutionary pressure to do so.
> "The speed at which nAb resistance develops in the population increases substantially as the number of infected individuals increases, suggesting that complementary strategies to prevent SARS-CoV-2 transmission that exert specific pressure on other proteins (e.g., antiviral prophylactics) or that do not exert a specific selective pressure on the virus (e.g., high-efficiency air filtration, masking, ultraviolet air purification) are key to reducing the risk of immune escape"
Doesn't this mean that the problem is in having a large number of infected individuals? Which is exactly what happens when a virus sweeps through the unvaccinated population - see, delta.
Also, since Covid and its variants seems to happily re-infect people who have already had it, the same evolutionary pressures will still be present, as long as there's a large reservoir of sick people, regardless of whether they are rubbing shoulders with vaccinated individuals, or 'caught it eight months ago' individuals.
We have two broad options for reducing the number of dangerous COVID mutations.
1. Harsh lockdowns, Australia/NZ/China style, to bring cases down. It works, but everyone hates it.
2. Mass vaccination, that gets us to herd immunity against the most prevalent strains of COVID, so that we no longer have millions of active cases. We're not there with 50% of the population vaccinated. We might be there if we were at 85%.
Since you seem to think that #2 is not the solution, what is your plan for stopping the evolution of the virus? #1?
1. https://jamanetwork.com/journals/jama/fullarticle/2782139
Your understanding of the situation differs by two and a half orders of magnitude from reality.
And that number has nowhere to go but up, as antibody levels in survivors drop.
i.e., the questionable number is orders of magnitude larger than the reliable number.
> as antibody levels in survivors drop
Recovered survivors have multiple mechanisms of defense, including antibodies against components of SARS-CoV-2 (not just spike protein) and T-cells, which have been proven effective against SARS1 after 17 years. They also have both nasal/mucous and blood/serum antibodies, unlike the vaccinated which have primarily blood/serum antibodies against one spike protein variant for symptom reduction.
Survivors don't need boosters. Those who take non-sterilizing intramuscular vaccines may need boosters.
The particular way requires both the original diagnosis of the first infection AND the diagnosis of the second infection to be done the same way.
Most infections never get diagnosed that way in the first place, which is why such a comparison is impossible for the vast majority of cases.
What exactly is your theory? That those 35,000 people never had COVID in the first place, or that what they got the second time around isn't COVID? Or that we can disregard every other word in that report, because the only word that matters in it is '137'?
> , which have been proven effective against SARS1 after 17 years.
Unfortunately for those people, we're not dealing with a SARS1 outbreak.
How many years have they been proven effective against SARS2?
> Survivors don't need boosters. Those who take non-sterilizing intramuscular vaccines may need boosters.
The science disagrees with your gut feeling. [1]
This is a false dichotomy, we have way more than two options. Below you'll find that I have supported my claim with exceptionally well cited publications and results from recent high quality clinical trials showing promising results.
A) strategies to prevent SARS-CoV-2 transmission that exert specific pressure on other proteins (e.g., antiviral prophylactics) [1][2][3][4][5][6]
B) strategies that do not exert a specific selective pressure on the virus (e.g., high-efficiency air filtration, masking, ultraviolet air purification)
C) Vaccines are absolutely part of the answer here. However, compulsory mass vaccination alone is exceedingly unlikely to be a solution - for all the reasons and evidence put forth in the citations of my previous comment - and because data from all over the world is showing that high vaccination rates alone are not preventing the dominance of VOCs [7][8].
[1] Multifaceted highly targeted sequential multidrug treatment of early ambulatory high-risk SARS-CoV-2 infection (COVID-19) https://scholarlycommons.henryford.com/cgi/viewcontent.cgi?a...
[2] Multidrug treatment for COVID-19 https://www.jstage.jst.go.jp/article/ddt/advpub/0/advpub_202...
[3] Ivermectin in combination with doxycycline for treating COVID-19 symptoms: a randomized trial https://pubmed.ncbi.nlm.nih.gov/33983065/
[4] Baricitinib plus Remdesivir for Hospitalized Adults with Covid-19 https://pubmed.ncbi.nlm.nih.gov/33306283/
[5] A review of therapeutic agents and Chinese herbal medicines against SARS-COV-2 (COVID-19) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7237953/
[6] Fluvoxamine: A Review of Its Mechanism of Action and Its Role in COVID-19 https://www.frontiersin.org/articles/10.3389/fphar.2021.6526...
[7] Update on Emerging SARS-CoV-2 Variants and COVID-19 vaccines https://www.cdc.gov/vaccines/acip/meetings/downloads/slides-...
[8] COVID-19 Science Update released: August 13, 2021 Edition 102 https://www.cdc.gov/library/covid19/08132021_covidupdate.htm...