> Hypothetically, if you were against banning of public gatherings to protect against COVID only the grounds that it violates 1a, if you were to repatriate in a country that didn't enshrine 1a, would your position on this policy change?

Great question. My reasoning would change, but my position would not. The issue is that the research I've done has convinced me that SARS-CoV-2 is literally the worst possible virus to lockdown over (and furthermore there's really not a virus out there where lockdown makes sense anyway).

BTW, the way we've done it in the USA is the worst of both worlds because we ate all the costs of containment, yet are actually practicing mitigation. It's like the opposite of the pareto principle.

Before I get into the health stuff, since we do have the 1A here, I will always argue the 1A over the health stuff, because arguing the merits of the policy on public health grounds means implicitly ceding the first amendment argument. Anyway, let's begin:

The reason I would still be against it if I were in, say, Europe, is because from a public health standpoint, I believe these measures worsen mortality over the long-term (and indeed the medium-term, and possibly even the short-term).

In short, this is because universal lockdown increases the proportion of at-risk people that must get sick before we hit herd immunity. Additionally, lockdown is going to reduce a population's sunlight exposure (Vitamin D is INCREDIBLY important for respiratory pathology, but nitric oxide is important too), it's going to reduce the amount people exercise/sleep, it's going to increase fear/anxiety, and it's going to decrease social interaction. Each of those individually are bad for the immune system, but taken together it's disastrous.

Severe COVID-19 seems to be an immunoregulatory disorder. You don't so much die from the virus as you do your immune response to the virus.

A virus like SARS-2, which is adapted to spread well (for example, it suppresses interferon in the early stages of infection which creates a ~2 day window of pre-symptomatic spread where viral load is high enough to transmit and yet there are no visible symptoms), but it is a very poor killer (even the CDC estimates a .65% IFR, and the CDC has a vested interest in using the worst numbers possible).

Furthermore the population targetted by SARS-2 is almost exclusively the very old or the very sick, which means the average years of life lost (YLL) per death is much lower than for Influenza, which actually does kill children in real amounts.

So in conclusion:

- the measures to slow spread don't seem to work to slow spread (this applies to universal masking btw)

- but insofar as those measures do slow spread, that's a bad thing, because it increases the number of high-risk
individuals that will get sick over the long-run, and

- of those who do get sick, if they've spent the last 3 months locked down they are more likely to die

BTW, since pre-existing exposure to non-SARS human coronaviruses produces T-cell cross-reactivity [1], we could have produced a pseudo-vaccine already by just dosing people with live non-SARS human coronaviruses.

[1] ["SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls"](https://www.nature.com/articles/s41586-020-2550-z) - Published: 15 July 2020

- Here, we first studied T cell responses to structural (nucleocapsid protein, NP) and non-structural (NSP-7 and NSP13 of ORF1) regions of SARS-CoV-2 in COVID-19 convalescents (n=36). In all of them we demonstrated the presence of CD4 and CD8 T cells recognizing multiple regions of the NP protein. We then showed that SARS-recovered patients (n=23) still possess long-lasting memory T cells reactive to SARS-NP 17 years after the 2003 outbreak, which displayed robust cross-reactivity to SARS-CoV-2 NP.

- Surprisingly, we also frequently detected SARS-CoV-2 specific T cells in individuals with no history of SARS, COVID-19 or contact with SARS/COVID-19 patients (n=37)