481–490 of 585 posts
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It hurts your case if you respond defensively or sarcastically.
Yes :(
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Only if you consider hanging out with someone a vaccine. As I mentioned in my reply to you it will be impossible to stop this strain from being deliberately spread by people on their own.
Wouldn't the same social distancing measures that keep the dangerous strain at bay keep the "good" one from spreading? And vice versa.
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In theory any coronavirus could, including the 4 we consider absolutely harmless. In fact, with existing attenuated virus approaches that eventually becomes the problem, the "last mile" of this approach usually sees you needing a real vaccine to cap off the disease. Otherwise the virus kinda circulates around in a tight enough cycle that you see most if not all eventual mutations including dangerous ones that kill. C…
The problem with polio back mutating is limited to one of the three strain in the live vaccine and is due to the mutations not being deletion mutations. The live polio vaccine was developed before people knew this and for regulatory reasons the problem has never been fixed. This problem is easy to avoid these days.
Personally I see your proposal as a relatively worthy endeavor to consider.
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These lower estimates are all estimates. Really it is not important from the perspective of doing something about this pandemic as a huge number of people will die at all estimated levels.
Maybe you can now correct the "killing between 1% to 3.5% of the people it infects" part. It's horribly misleading. IFR < CFR and IFR estimates go always down over time and never up due to the skewed nature of the data. Antibody tests are coming in already and based on them you get very accurate numbers.
TLDR the virus mutates too quickly for this to be safe.
" There are many ways to make vaccines, and the oldest one is to take the wild-type pathogen, and either ‘break’ it (‘attenuate it’), or find an example in nature that’s messed up and can’t cause disease.
The initial smallpox vaccine was cowpox: Close enough to human smallpox that it elicited protective immune responses, but too maladapted to humans that it couldn’t thrive in us, and would be caught by the slow-walking cops of our immune system.
The strategy used for many of the 1950s/60s-era vaccines was to isolate the disease-causing pathogen, then in a laboratory force it to grow in progressively more-messed-up circumstances. This would drive evolution of the pathogen to mis-adapted freaks. For example, the mumps isolate was from the daughter of the Merck scientist (Maurice Hilleman), and he grew it in cow cells, then lizard cells, then insect cells (or somesuch, I don’t know exactly). By the end of the process, the thing could still infect humans, but just BARELY.
Nowadays, with molecular biology, we can rationally design the ‘attenuations’, and do knock-outs or modifications.
Which brings me to low-virulence wildtype isolates of SARS-CoV-2 (S2): The root problem here, as with HIV, is it’s a super-fast-evolving RNA virus. Sure, a particular isolate might be low-virulence NOW, but give it a few weeks on a cruise ship and – viola! – nasty bugger ahoy!
When SARS-CoV-1 broke out, years back, it had a high lethality and freaked out the public health experts at the time (in fact, we were writing proposals to get into the research, but then it got contained). At that time, efforts were initiated to make a vaccine, based on the observation that all that was needed with the Bcell production of ‘neutralizing antibodies’. This is the long standard, matching most existing vaccines. So it was a low-weight lift, for vaccine developers (relatively easy-peasy). The project got pretty far along, but then stopped when SARS-CoV-1 disappeared as a threat.
When MERS, then SARS-CoV-2 came along, they resurrected the previous, promising design, based on a slow-evolving vector. But in the case of S2, they discovered that the targeting receptor usage of S2 was significantly different, so the design required a significant re-tune. Even so, the Chinese (I think) did it, injected the first people several weeks back, and I don’t think it works well (too early for formal reports).
S2 is nasty, as HIV is. It is using evolution against us. And because its hypermutable (like the influenza viruses), it’s going to be nearly impossible to make one vaccine that works cycle after cycle. It will continue to evolve, but the subsequent cycles will probably have lower lethality than this first pass (which was completely novel to the human immune system, so we had no ‘herd immunity’ protection). Going forward, it will be hard for highly-virulent forms to transmit if they kill their hosts too quickly, which will select for less-virulent forms.
The trick is to stay alive during this pass. The only mechanism we have to do this is to not get infected. The only way to do that is to not expose ourselves to infected people, or the things they’ve touched.
We’re back to how things were in the 1800s. Better than no science, but about the same as post-epidemiology/cell-theory-of-disease (1890s)
But as I said, this vaccine should be RELATIVELY easy to develop. It doesn’t have to be perfect, it just has to blunt viremia (so that the global pneumonia it causes in your upper/lower respiratory system doesn’t cause aveoloar collapse. In other words, even working a little bit will probably massively lower the death count.
But even an easy-peasy vaccine will take 18 months. There’s just no getting around that, unless you want to inoculate 5 billion people with something that might make the pandemic worse."
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Even better than pooling is griding [0]. 0. https://twitter.com/rwade300/status/1247340350076628992
If B2 and D4 are positive, then in the marginals B,D,2,4 will show positive, but you don't know which of B2, B4, D2, D4 are positive.
If you get ambiguity then you just move those samples across to a new grid (in locations that won’t be ambiguous) and test again.
> Singapore and Japan have recently seen this in action where they eased restrictions and found the disease came back and they had to reintroduce restrictions. Poorly informed, Japan did not even have restrictions in the first place.
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If we wait for the long term we will all get infected and we will all be broke. We need to think differently. I am not arguing that we should infect people on purpose. If people chose to become infected on their own by hanging out with those infected with an attenuated strain then that is a very different legal question. Personally I think the result would be the regulatory agency would just rush the use through base…
Here's what I have trouble reconciling: You say that this attenuated virus would spread automatically -- just like a virus -- and yet no one would be infected on purpose, only if people "chose to become infected on their own by hanging out with those infected with an attenuated strain". How much agency do I have in whether I get infected or not? It seems strange to me if it depends on the genetic makeup of the virus.
This discussion is really a distraction as I don’t think a “grass roots” spread would be the way any such strain would be spread. I think the regulatory agencies would look at the data collected from the natural spread and use this to approve the strain for use.
He leaves out "developing a treatment" as an option. Why?
The author doesn't address how widespread the testing would need to be to accomplish this. What sample size is needed? Does it need to be geographically diverse? Does the human population tested need to be genetically diverse? Also: Why is this faster than other methods of vaccine development already underway? Once developed, wide-scale manufacture & deployment is an enormous logistical challenge completely separate…
The reason why this would be faster is the process of looking for the strain and identifying it as safe would generate data that would allow the regulatory authorities to approve its use.
Manufacturing would not be the limiting factor here.