Impossible to ever know, but my money would be on human-to-human transmission during the handover, either directly during conversation or by handling the pet-carrier.Originally Posted by Trebuchet
Grant Hutchison
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Impossible to ever know, but my money would be on human-to-human transmission during the handover, either directly during conversation or by handling the pet-carrier.
Grant Hutchison
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Pandemic reaches Antarctica, last untouched continent. Chilean authorities announced that at least 58 people that were at two military bases in Antarctica or on a navy ship that went to the continent tested positive for the new coronavirus.
https://apnews.com/article/pandemics...bca98bf5833cf5
Do good work. —Virgil Ivan "Gus" Grissom
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Another new variant of COVID-19 is spreading rapidly in South Africa.
https://www.cbsnews.com/news/covid-1...africa-spread/
Do good work. —Virgil Ivan "Gus" Grissom
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Remember when this thread started, we were so worried about Zika virus and Ebola? Those days seem so distant now...
"I'm planning to live forever. So far, that's working perfectly." Steven Wright
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And yet, African Swine Fever kills virtually 100 percent of pigs with the severe strain.
The moment an instant lasted forever, we were destined for the leading edge of eternity.
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The diseases have not changed. The priorities have changed.
"I'm planning to live forever. So far, that's working perfectly." Steven Wright
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Evolution happens, change is to be expected. Even bacteria in remote caves develop antibacterial resistance just by competing with each other. Life is a dynamic meta stable state of complexity. We are living through another phase where we can sequence the evolving genome. So another chapter opens.
sicut vis videre esto
When we realize that patterns don't exist in the universe, they are a template that we hold to the universe to make sense of it, it all makes a lot more sense.
Originally Posted by Ken G
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But the point was, those threats have not gone away or become less virulent. They simply stopped making headlines because now we have something even more serious and threatening to compare them to.
"I'm planning to live forever. So far, that's working perfectly." Steven Wright
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Why is there such a broad human response to this novel coronavirus? I mean, some people die from it (not all of whom have co-morbidities), some people get really sick ("...sicker than I've ever been"), some people get mildly sick, and apparently some people get barely sick at all. This just doesn't make a lot of sense. I can understand that some people's immune system response is better than others, but still, is that all there is to it?
Everyone is entitled to his own opinion, but not his own facts.
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I'd say this sort of spectrum of response is actually pretty common--it's just that, unless you're a friend or family member, you don't normally hear about all the people in intensive care who suffer a life-threatening reaction to a generally benign disease. The sheer prevalence of Covid has brought the existence of a "severe disease" tail for this infection into the spotlight, but that sort of thing has been going on in the background for as long as humans have existed.
For instance, some of the sickest people I ever dealt with had Group A Streptococcal disease--an overwhelming inflammatory response to a pretty much ubiquitous and generally mild pathogen.
What we've started to see is that these people are generating a disordered immune reaction to a specific provocation, and that this has specific genetic associations. Some of the genetic associations for Group A Strep disease were published this year. And the same thing has been turning up with Covid--a couple of weeks ago Nature published "Genetic mechanisms of critical illness in Covid-19".
So basically there are a group of people who probably get a high viral load to begin with, and then mount a disordered immune response (the "cytokine storm" that you may have heard of).
Grant Hutchison
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Since this is a completely new human vaccine technology (mRNA), has it been thoroughly tested for safety? Or will we add it to such treatments as thalidomide, bextra, vioxx, baycol, rezulin, darvon, phenylpropanolamine, posicor, fen-phen, seldane, Diethylstilbestrol, accutane, duract, omniflox, and palladone?
SHARKS (crossed out) MONGEESE (sic) WITH FRICKIN' LASER BEAMS ATTACHED TO THEIR HEADS
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It has, yes.
Grant Hutchison
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mRNA vaccines did spring out of nothing in the last year, but are built on 30 years of research
Harvard.edu
wikipediaSo, 30 years of painstaking research allowed several groups of scientists — including a group at Pfizer working with a German company called BioNTech, and a young company in Massachusetts called Moderna — to bring mRNA vaccine technology to the threshold of actually working. The companies had built platforms that, theoretically, could be used to create a vaccine for any infectious disease simply by inserting the right mRNA sequence for that disease.
Researchers at the Salk Institute, University of California-San Diego, and a US-based biotech company, Vical Incorporated, published work in 1989 demonstrating that mRNA, using a liposomal nanoparticle for drug delivery, could transfect mRNA into a variety of eukaryotic cells.[13] In 1990, the University of Wisconsin, reported positive results where "naked" (or unprotected) mRNA was injected into the muscle of mice.[3] These studies were the first evidence that in vitro transcribed (IVT) mRNA could deliver the genetic information to produce proteins within living cell tissue.[3]
The use of RNA vaccines goes back to the early 1990s. The in vitro demonstration of mRNA in animals was first reported in 1990,[14] and use as immunization proposed shortly thereafter.[15][16] In 1993, Martinon demonstrated that liposome-encapsulated RNA could stimulate T-cells in vivo, and in 1994, Zhou & Berglund published the first evidence that RNA could be used as a vaccine to elicit both humoral and cellular immune response against a pathogen.[3][17][18]
Hungarian biochemist Katalin Kariko attempted to solve some of the main technical barriers to introducing mRNA into cells in the 1990s. Kariko partnered with American immunologist Drew Weissman, and by 2005 they published a joint paper that solved one of the key technical barriers by using modified nucleosides to get mRNA inside cells without setting off the body's defense system.[3][19] Harvard stem cell biologist Derrick Rossi (then at Stanford) read Kariko and Weissman's paper and recognized that their work was "groundbreaking",[19] and in 2010 founded the mRNA-focused biotech Moderna along with Robert Langer, who also saw its potential in vaccine development.[19][3] Like Moderna, BioNTech also licensed Kariko and Weissman's work.[19]
Established Member
I will be 63 March 5. I have Asperger's and am overweight (used to be obese), but have no other co-morbidities. I live in Ohio.
When might I get my jabs? March? April? The merry, merry month of May?
SHARKS (crossed out) MONGEESE (sic) WITH FRICKIN' LASER BEAMS ATTACHED TO THEIR HEADS
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Depends on vaccine supply, and your state's clinical priorities, which have yet to be established for under-65s. I suggest you monitor the vaccination distribution page for Ohio.
Grant Hutchison
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Thanks, grant!
Bookmarked in my favorites.
SHARKS (crossed out) MONGEESE (sic) WITH FRICKIN' LASER BEAMS ATTACHED TO THEIR HEADS
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The Christmas surge in new USA cases seems to have settled down a bit, with the 7-day average running under 200,000 cases daily where it had been well above a couple of weeks ago. But now we are seeing the resultant surge in deaths. It's a mess.
Cum catapultae proscriptae erunt tum soli proscript catapultas habebunt.
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Are the new vaccines effective against the new, supposedly more deadly virus? Or will we need a new Operation Warp Speed?
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The evidence is that the vaccines are equally effective against the English variant, but may have some reduced effectiveness against the Brazilian and South African variants, which have more spike mutations. That information is currently coming from testing antibodies from vaccinated people against viral samples in the laboratory, but the definitive test is to see what sort of protection vaccinated people have in the real world--stuff you can detect in the laboratory sometimes doesn't actually turn out to make much difference in the epidemiology. If there is reduced effectiveness, it's likely to show up (as my linked article states) with vaccinated people developing a mild or asymptomatic dose of Covid, while still being protected from hospitalization or death.
As to the "more deadly" label that the English variant has just acquired--there's conflicting evidence that's still shaking down. The UK's Chief Scientific Adviser reported today that people hospitalized with the new variant are no more likely to die than with the "old" variant, but that there's also epidemiology suggesting that people who test positive for the new variant are slightly more likely to die than those with the old variant. It's difficult to reconcile those two results, unless susceptible people have some reason to die without hospitalization (frail care-home residents, for instance). The picture should get clearer as more data come in. But if there really is a difference, I have a 1% chance of dying if infected with Classic Covid, and a 1.3% change of dying from new Covid. "More deadly" needs some perspective, and the media's translation of this into "30% more lethal" is unhelpful, to say the least.
Finally, we're not going to need another Operation Warp Speed (thank God, what a dumb name). The existing mRNA vaccines are easily adapted to produce the new spike proteins, and they won't need to go through large Phase III trials again if that's required. (Just as your ever-changing yearly flu vaccine doesn't go through new trials every year.) I've read industry representatives saying that it would take a couple of months to retool for a new variant of the existing vaccine.
Grant Hutchison
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Did anything come of the anecdotal evidence that smokers or people who wear eyeglasses are less likely to contract COVID-19?
New Jersey recently classified smokers as a "high risk medical condition" for vaccine receipt, so perhaps there was nothing to the smoking claim?
I may have many faults, but being wrong ain't one of them. - Jimmy Hoffa
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The evidence for smoking reducing Covid risk went well beyond anecdotal--there was a lot of early epidemiology showing a reduced prevalence of smokers among hospitalized Covid-19 patients, and there was a reasonable hypothesis for biological mechanism (the "nicotinic hypothesis"). The French trial of nicotine patches in severely ill Covid patients is still ongoing. Unfortunately, there were many potential sources of bias in the early reports--they relied on patient's self-reporting of smoking status, didn't look at recent smoking history, didn't seek a dose-response relationship, didn't use objective measures of smoking status (like carboxyhaemoglobin levels), and so on.
So people began to worry that we might be seeing a repeat of the so-called "smoker's paradox" with regard to survival of myocardial infarction--better data made the apparent paradox go away. But no-one seems to have done the definitive study yet, as far as I can see.
The New Jersey decision seems odd, given that the risk from smoking is going to be related to the diseases caused by smoking--cardiovascular and respiratory conditions which are already on their "high risk" list.
The eyeglasses thing is pretty much anecdotal, however. There are plausible mechanisms by which that might work, but only (literally) if you're within spitting distance of an infected person.
Grant Hutchison
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An interesting analysis in The Lancet this week, The relationship between cultural tightness–looseness and COVID-19 cases and deaths: a global analysis, which discusses something we touched upon in this thread early last year.
The authors use a pre-existing measure of cultural tightness/looseness (in effect a culture's tendency to follow rules and norms), and compare that to Covid cases and deaths, while controlling for a number of other variables. Basically, the looser your society, the worse you've fared with this pandemic (with a lot of scatter).
Some of the proximities in the graphs are interesting--Sweden and Singapore have similar estimates of tightness/looseness, and plot right next to each other for cases, but extremely far apart for deaths. I suspect that reflects how Sweden's outbreak hit care homes badly, but Singapore's hit migrant worker dormitories.
Grant Hutchison
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Okay, this article is posted on Yahoo news, and my British news filter isn’t properly calibrated to know how much credence to afford The Telegraph, but if there is anything to this, some Israeli doctors may be onto an effective treatment for COVID-19.
https://www.yahoo.com/news/israeli-c...191709164.html
I may have many faults, but being wrong ain't one of them. - Jimmy Hoffa
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Dailymail has more information than that article . . . which is frightening (I’ve heard that paper referred to as “Dailyfail”). Here’s the article:
https://www.dailymail.co.uk/news/art...-hospital.html
It wasn’t a double blind study and it hasn’t been published anywhere, so there isn’t much to go on. It also had a small number of participants. A small sample size, 29 out of 30 were said to improve more quickly than expected, but there is no current information on ages, other treatments taken and so forth. It is apparently an immune modulator drug taken by inhalation, thought to reduce an overreaction to the infection and improve lung function. So, perhaps interesting enough to look into further, but don’t get too excited.
"The problem with quotes on the Internet is that it is hard to verify their authenticity." — Abraham Lincoln
I say there is an invisible elf in my backyard. How do you prove that I am wrong?
The Leif Ericson Cruiser
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It sounds cool, and I hope it turns out to be true. One caveat is that this seems to be "science by press release," because I haven't been able to find a peer-reviewed paper on the study, though that may just be a failure of my search skills.
Also, just as an interesting point, like interferon beta, the active ingredient in the drug is a protein called CD24, which is a natural signaling molecule which somehow modulates immune response. So what is kind of nice about that it that unlike drugs that target specific proteins of the COVID virus, this is something that I think could potentially be used for any virus that causes this kind of runaway inflammatory reaction. Apparently it was originally made for cancer.
As above, so below
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No, the article I linked above said it hasn’t been published in any journal, which is why I mentioned it hadn’t been published. There have been a lot of stories like that around COVID-19, mentioning preliminary results with minimal data.
"The problem with quotes on the Internet is that it is hard to verify their authenticity." — Abraham Lincoln
I say there is an invisible elf in my backyard. How do you prove that I am wrong?
The Leif Ericson Cruiser
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Sorry, yeah that's what I get for not reading through the whole thread before responding.
As above, so below
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Why (in simple terms) will I need TWO shots? Why not one or three?
SHARKS (crossed out) MONGEESE (sic) WITH FRICKIN' LASER BEAMS ATTACHED TO THEIR HEADS
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For the two-dose vaccines, the first shot sensitizes the immune system, but does not provide full protection. The second shot kicks up the response to a much more effective level, assuring longer term protection.
"I'm planning to live forever. So far, that's working perfectly." Steven Wright
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In simple terms--because that's just the way it is.
We're not at the stage of being able to predict the immunogenicity of particular vaccine candidates (though we do have a good idea of what works and what doesn't). So one of the things that happens in Phase I trials (small numbers of volunteers) is that the immune response to various dose regimens is tested. The manufacturer then makes a decision about the best regimen, and that isn't as simple as just going for the best immune response--there's no point in producing a complex multidose schedule if (as we know) people are a bit rubbish about remembering to get later doses of the vaccine.
So the J&J vaccine produced such effective immunity after a single dose, they decided to go with that regimen, because from a public health point of view that actually might prove more effective at limiting disease transmission than a two-dose regimen in which a significant number of people fail to get the second dose.
In general, multiple doses are used because they produce an increment in immunity and longer-lasting immune memory. The first dose primes the immune system, the second nudges it to say, "This is going to be a recurring problem, better remember this set of antigens."
Beyond that, we need longer experience than we've had with Covid to see if subsequent doses are required to maintain immune status. Tetanus toxoid, you may recall, involves three doses initially and then subsequent doses at ten year intervals up to a total of five or six. So we needed decades of experience to figure that one out, and it only works because people tend to have injuries that need medical attention on that time scale, so they're a recurring captive audience for their booster shots.
Grant Hutchison
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