I don't know your story, so apologies if this is too presumptive or doesn't make sense: To what extent do you feel the same person more-actualized, as opposed to a new person, born after coming out?

The best I could do is Rhode Island, which is basically a city.

https://civiqs.com/results/embed?snapshotUrl=production-model-results.civiqs.com/snapshots/2060a11d-7421-4fba-b1cf-5034385a275e

https://civiqs.com/results/embed?snapshotUrl=production-model-results.civiqs.com/snapshots/aba6b473-6389-47ab-9ac8-242ea0c2afc2

Still there.

Maybe compare North Dakota Dems to Rhode Island Republicans?

https://civiqs.com/results/embed?snapshotUrl=production-model-results.civiqs.com/snapshots/e3b661b4-b4c4-405e-9760-765d46bd2ebb

Dems are still more concerned.

My guess is that this holds up, even if your sample population is from the same rural or urban area.

Actually, I am now skeptical. The reasoning seems circular. The pangolin theory seems based upon the fact that although the bat virus RaTG13 is 96.12% identical to SARS-Cov2, the pangolin-CoV has the ACE2 site, and is 91.02% and 90.55% identical to SARS-CoV-2 and BatCoV RaTG13.

https://www.ncbi.nlm.nih.gov/pubmed/32197085

And the above authors are saying that since the S1 in pangolin is closer to SARS-Cov2 it must have had a gain of ACE2 binding in humans. But what about the 96.12% identical RaTG13? Is it possible that someone was messing with RaTG13 and drove a mutation that resulted in ACE2-binding?

And here is that backbone (MG772934 and MG772933) being collected and grown in rats and human cells in 2018:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6135831/

In this study, a suckling rat model was initially used to study the possibility of the proliferation of bat-derived CoVs in other animals. Previously, only one report had shown promising results associated with the isolation of live SL-CoVs from the fecal samples of bats with Vero E6 cells13. The live SL-CoV cultured in Vero E6 cells presented a typical CoV morphology and has the ability to use ACE2 from humans, civets, and Chinese horseshoe bats for cell entry33. An attempt to isolate the virus with Vero E6 cells was unsuccessful, which was likely due to a low viral load or a lack of compatibility with Vero E6 cells. This study found that the SL-CoVs derived from bats could replicate successfully in suckling rats, and pathological examination showed the occurrence of inflammatory reactions in the examined organs of the suckling rats. This result indicated that the virus can proliferate in rats and has the potential of cross-species transmission. When CoV particles procured from the infected brain tissues of the rats were studied by electron microscopy, the morphology of the particles was found to be identical to the typical coronavirus particles, as described in previous studies34. However, the typical spikes could not be visualized by electron microscopy. This observation can be partially explained by the hypothesis that the S1 and S2 domains of the S protein (which are not well-connected) were easily detached from the virion using excessive freeze-thawing or ultracentrifugation6.

Also, rat ACE2, not crazy different from human ACE2. This from 2005.

By altering histidine 353 in rat ACE2 and modifying a glyosylation site that may alter the shape of a-helix 1, we converted rat ACE2 to an efficient receptor for SARS-CoV.

Ok, I am descending into #mkbatshittery. I need to stop.

Here's the article.

In short, they assume it is most likely from pangolins, with the gain of human ACE2 binding to have happened in humans. They do not think someone designed the ACE2 site with a program, because it is not a predicted high-efficiency ACE2 site using software.

All SARS-CoV-2 genomes sequenced so far have the genomic features described above and are thus derived from a common ancestor that had them too. The presence in pangolins of an RBD very similar to that of SARS-CoV-2 means that we can infer this was also probably in the virus that jumped to humans. This leaves the insertion of polybasic cleavage site to occur during human-to-human transmission.

The authors note that this gain of function could feasibly have been the result of driven mutation in the lab.

The acquisition of polybasic cleavage sites by HA has also been observed after repeated passage in cell culture or through animals.

However, this coronavirus isn't a with a commonly used backbone. That is, researchers haven't been messing with it and publishing the results.

Thus, the ACE2 site isn't one your computer would tell you to use, and the virus itself isn't a coronavirus known to be used by scientists. Therefore, the authors conclude that the virus probably went from pangolins to humans, and then gained the ACE2 site.

This is a very good point. I’m going to see if one can normalize for rural/urban.

That looks simply amazing.

I agree that there is no reason to rush in. I expect the Dow to dip below 13,000 before the bottom.

Martha Gellhorn was a badass that got fed up with his shit.

I love Hemingway's short stories, however. Remove his flaws, and they would suck.

LOL it's like everything that everyone's grandmother told them to take when they are sick, but in one pill.

Furin activity exposes the binding and fusion domains, essential steps for the entry of the virus into the cell. Since the S- glycoprotein of all coronaviruses contains a similar furin cleavage site, it is plausible that the activity of this enzyme is essential for the zoonotic transmission of many coronaviruses, including Covid-19 enveloped by a MERS-CoV and Sars-CoV S glycoprotein containing a furin cleavage site.

...

In these perspectives, likely, targeting furin might be an option for the prevention or treatment of Sars-CoV2 infection.

So yeah. Maybe inhibiting furin will work. The author theorizes it might help even more so in patients with heart issues.