Many aren't aware but interestingly these variants are identified and designated in the open on GitHub, here is the GitHub issue for this B.1.1.529 designation https://github.com/cov-lineages/pango-designation/issues/343. I've recently started watching this repo as it's quite interesting reading about the different variants popping up across the world.
This GitHub repo is just about registering the Pango lineage, based on data already collected and published at other locations.
1. Viruses are constantly mutating, its kind of their thing.
2. Most mutations do absolutely nothing or are actually harmful to the virus.
3. When a new mutation is noted to be spreading fast its usually because of the nature of super spreader events and not because the new mutation is more or less transmissible.
4. Scientist and health officials should absolutely be keeping an eye on these things.
 Vincent Racaniello - SARS-CoV-2 UK variant: Does it matter
For this new variant it could still plausibly be a founder effect. But that's because the circumstances are different this time (the variant became dominant while cases were surging from almost nothing, not when the cases were already at a high level). Not because that checklist is actually correct.
Claiming Vince was wrong in the video also means the researchers that discovered the variant were wrong. After all he was just parroting their findings in the video.
Yeah, that's a virology point of view all right. That something has to have a proven biological mechanism before it can be taken as fact, or even considered as a risk. That's bad public policy though. With his reasoning there would have been no reason to increase restrictions in the UK in Dec/Jan, but in fact the restrictions were extremely necessary and the variant caused tens of thousands of extra deaths.
Also the claims about variants being "more infectious" are - when you dig in - hopelessly confounded by seasonal effects that many epidemiological papers were at that time still ignoring.
For your seasonal effect explanation to make any sense, the effect would have to have only applied to Alpha but not to baseline Covid at the same time. And then it's not a seasonal effect, is it? It's an actual difference in the behavior of the two variants. The same goes for any other similar confounder that you try to manufacture.
Is there any evidence besides an appeal to authority?
My mother at 14 after a car accident was considered as lost cause and by opinion of expert she should be dead, but survived only because her relative with much less medical expertise believed in second opinion and got her in different hospital. Sometimes, these stupid parroted ideas about expert opinions can only be proven wrong by personal experience only. But quite many people do not learn from their own mistakes, so, meh - there is no cure for stupid people, who can't think by themselves.
PS Every covid mutation so far has put scientists on alert...
Is that the case here?
There’s an overlap with hard left and a few other niche political views as well. Though with less victimhood and more consistency at times.
Personally, I care very little for appeal to authority myself. The bias among experts based on their political views is generally going to be very high.
I assign higher priors to subject matter experts until I have reason to believe otherwise.
I mean, it is a logical fallacy. An expert isn't right only because he's an expert, he's right only when the evidence supports his position. Do all experts only make conclusions based on evidence, or do other beliefs factor in? I think the answer is clear, hence the fallacy.
For any given scientific question, select two populations. One populaton is enriched in subject matter experts, while the other is selected at random. Have them make blind predictions about scientific facts. It is not fallacious to sdtate that the first group's predictions will have a higher posterior probability.
Source: Myself, an authority
Joking aside, you are just misrepresenting what the "appeal to authority" logical fallacy is. An "appeal to authority" is when one argues that "X is correct because <insert some expert> said it was". In really, X is either correct or incorrect, regardless of what any authority has said about it.
So yes, appeal to authority is absolutely a logical fallacy. Changing the definition of those words and then arguing that your definition isn't a fallacy is called a fallacy of equivocation. And yes, a fallacy of equivocation is also a logical fallacy.
That's not the only kind of argument that exists though, and we're pretty unlikely to be in that kind of argument on the internet talking about current events. When trying to tell from incomplete facts what's more likely to be true, listening to what an expert says is a pretty good start.
But yeah, I like the way you put this; we're just arguing on the internet about things which are too messy to have a true false dichotomy.
Logic is part of math, and logic is where logical fallacies come from.
To which you replied: "Vincent Racaniello is a professor of virology.
This is an appeal to the authority of Vincent's position as a professor
When asked for evidence, the ONLY evidence that you provided, was that he IS an expert. Full stop.
Comment. My 2nd reply with link.
The parts of the video where he literally quotes the original findings.
It's a bit unfair that the GP calls him Vince from Youtube. He's a professor of virology so not just some nobody giving his opinion on Youtube. This doesn't mean he can't be wrong of course.
But all good. I used to listen to his podcast at the beginning of the crisis but after a while I stopped because I felt they were ignoring reality while waiting for science. Which felt like a strange way of working when reality was what we had to base decisions off of.
because the science matters. This new SA variant could be more transmissible or it could not be. Lets stick to the actual data and go from there.
Stop shoveling carbs at every meal. Lose 30 pounds. Start to exercise and increase cardio-pulmonary performance.
It appears most people in developed countries became couch potatoes and gained fat.
To each his own. My body, my choice. Your body, your choice.
Delta’s quick growth rate has been especially dramatic, says F. Perry Wilson, MD, a Yale Medicine epidemiologist. Delta was spreading 50% faster than Alpha, which was 50% more contagious than the original strain of SARS-CoV-2, he says. “In a completely unmitigated environment—where no one is vaccinated or wearing masks—it’s estimated that the average person infected with the original coronavirus strain will infect 2.5 other people,” Dr. Wilson says. “In the same environment, Delta would spread from one person to maybe 3.5 or 4 other people.”
“ We found a mean R0 of 5.08, which is much higher than the R0 of the ancestral strain of 2.79.”
Please stop spreading misinformation.
This claim is wildly false, and you've already been refuted by someone else.
Remove your false post.
Mostly true but in some very major cases it was because the variant did spread faster in general. Such as Delta and the British variant before hand.
Basically superspreader events can artificially boost a variant for a bit -- it is basically noise. You need to look at a longer time frame to be sure.
I think the process that you’re describing is the process of genetically evolving-by-mutation life forms in general. So not specific to viruses.
Human bodies are the vehicles for our genes to survive and reproduce :-)
Viruses don't have goals. If a virus successfully makes more virus, then there is more of the virus. For viruses that don't do that, there are less of them. That's all there is to it.
It so happens that making more virus often requires resources that were previously in use by other organisms. But that's incidental, not by design.
You only see viruses that are good at making more virus because the other ones died out.
If they're too successful at what they do their host dies before they can be passed on, if they're not successful enough then the infection wave loses momentum and dies out. Effectively we have been helping them for the last year and a half do do this, without our help this particular virus would die out within a couple of weeks. It needs us for transportation and to be brought in contact with new viable hosts. On its own it can't do much of anything.
Native copper ore got largely picked up and used by humans rendering such deposits "extinct" from early civilizations and lead to the practice of mining after the low hanging fruit was used up.
Killing your host is an awful strategy for continued existence if you don't have your own lipid bilayer.
The virus does not decide a strategy, it is random mutation and selection and even if it is less likely it might be that we could have a variant that is super transmissible and super deadly. This effect could be obtain in the delay between transmission and visible effects on human body. Example: virus is transmissible with N days before we can see signs of infection.
Of course we can fight back by testing everyone weekly even if they show no signs.
Help me understand how a virus can replicate without being detected but can also increase its lethality.
We already have an asymptomatic and infectious incubation period. If that kept stretching longer then you are delaying the lytic cycle even longer? Or does propogation and ultimately viral load also happen as a slower burn? Eventually you will have damaged too many cells.
I am not up to date with latest research but it seemed to be that SARS-CoV-2 is a virus that can be transmitted before symptoms onset.
Regarding replication without being detected but also increased lethality this you might be right that doing the math maybe the hypothesis I present seems far fetched.
Still I guess that a slight bump in mortality will create a lot of deaths due to its transmission.
Of course like I said I am just expressing an opinion that might be very wrong.
No virus has ever done this.
This is why Flu shots are seasonal
People are developing mRNA vaccines for 'flu now. Moderna, Pfizer and Sanofi all have mRNA 'flu vaccines in clinical trials, and there are a bunch more in the pre-clinical stages.
It's designed to make a statement, rather than elicit information. (Ref Oxford Languages).
The point of vaccines is not perfection but more like a war of attrition. A vaccine has several potential purposes, some of them are these:
* Reduce the possibility of infection
* Reduce the effects of an infection
* Reduce the infectiousness of an individual to other people
Each of those items above have various probabilities associated with them and rather a lot of external factors and so on. A vaccine's stated effectiveness in each area will obviously be some sort of average across a population.
That's the thing: Vaccines inoculate societies as a whole and not just individuals when you look at statistics. The phrase "anecdotes are not data" is particularly true here.
Even a "lol sad" 40% effective (whatever that means) vaccine will slow the spread of the thing across a population and reduce the possibility of individual deaths or other non optimal outcomes. When you start to look at the population as a whole you see huge numbers of people living instead of dying.
With luck, one of those survivors might be you or me one day. This is the only time I will advocate a sort of communist approach to things. By "risking" inoculation, you reduce the possibility that someone else might catch the disease. You also get some additional abilities to fight off the bloody thing too - nice!
Definitely a better outcome than not getting a flu shot.
> something that doesn't bother me
Yeah you've never been unlucky enough to get a bad flu.
I'll absolutely choose the "constant hassle" of getting a flu shot (i.e. a 5 minute pit stop at the drug store once per year).
The flu sucks.
How Flu Viruses Can Change: “Drift” and “Shift”
Influenza (flu) viruses are constantly changing. They can change in two different ways.
One way flu viruses change is called “antigenic drift.” Drift consists of small changes (or mutations) in the genes of influenza viruses that can lead to changes in the surface proteins of the virus, HA (hemagglutinin) and NA (neuraminidase). The HA and NA surface proteins of influenza viruses are “antigens,” which means they are recognized by the immune system and are capable of triggering an immune response, including production of antibodies that can block infection. The changes associated with antigenic drift happen continually over time as flu viruses replicate (i.e., infect a host and make copies of themselves). Most flu shots are designed to target the HA surface proteins/antigens of flu viruses. The nasal spray flu vaccine (LAIV) may target both the HA and NA of a flu virus.
The small changes that occur from antigenic drift usually produce viruses that are closely related to one another, which can be illustrated by their location close together on a phylogenetic tree. Flu viruses that are closely related to each other usually have similar antigenic properties. This means that antibodies your immune system creates against one flu virus will likely recognize and respond to antigenically similar flu viruses (this is called “cross-protection”).
However, the small changes associated with antigenic drift can accumulate over time and result in viruses that are antigenically different (further away on the phylogenetic tree). It also is possible for a single change in a particularly important location on the HA to result in antigenic drift. When antigenic drift occurs, the body’s immune system may not recognize and prevent sickness caused by the newer flu viruses. As a result, a person becomes susceptible to flu infection again, as antigenic drift has changed the virus’ antigenic properties enough that a person’s existing antibodies won’t recognize and neutralize the newer flu viruses.
Antigenic drift is an important reason why people can get flu more than one time. Drift is also a primary reason why the composition of flu vaccines for use in the Northern and Southern Hemispheres is reviewed annually and updated as needed to keep up with evolving flu viruses.
Another type of change is called “antigenic shift.” Shift is an abrupt, major change in a flu A virus, resulting in new HA and/or new HA and NA proteins in flu viruses that infect humans. Antigenic shift can result in a new flu A subtype. Shift can happen if a flu virus from an animal population gains the ability to infect humans. Such animal-origin viruses can contain HA or HA/NA combinations that are different enough from human viruses that most people do not have immunity to the new (e.g., novel) virus. Such a “shift” occurred in the spring of 2009, when an H1N1 virus with genes from North American Swine, Eurasian Swine, humans and birds emerged to infect people and quickly spread, causing a pandemic. When shift happens, most people have little or no immunity against the new virus.
While flu viruses change all the time due to antigenic drift, antigenic shift happens less frequently. Flu pandemics occur rarely; there have been four flu pandemics in the past 100 years. For more information, see pandemic flu. Type A viruses undergo both antigenic drift and shift and are the only flu viruses known to cause pandemics, while flu type B viruses change only by the more gradual process of antigenic drift.
Meanwhile rest of the world hasn't got their first dose of a reliable vaccine.
If rest of the world don't want it, I'll take it (and did).
The only way to keep cases to a low enough level to be successfully 'processed' by the health system is to maintain fairly severe social restrictions - and maintain them forever.
I believe that all of our successful vaccination campaigns (against highly contagious viruses) have by necessity resulted in (near) eradication. E.g. Polio, Smallpox, Measles, Rabies (in animals)
The slogan "Gotta catch 'em all!" makes that idea even less viable than it first seems.
I think most Americans have at this point enough exposure to news about China that they'd pronounce it "she", as if it were pinyin. In the fraternity/sorority system, I think most people pronounce it "zai", but my understanding is "k'see" or "ke-see" is closer to classical (and perhaps modern) Greek pronunciation.
I had an analogue control systems professor with a very strong accent (his catch phrase was "Quitch dewice wuh you choose?") who pronounced Xi close to correctly. I presume a huge chunk of the class (about half of the men, and many women at MIT were in fraternities/sororities/independent living groups at the time) probably dismissed his pronunciation of the Greek due to his accent in English and their prior exposure to the Greek alphabet in the "Greek" living system.
Naming a disease after private intellectual property is a terrible idea. Im not sure what that would accomplish.
Look here then:
Increased risk [compared to non-variant-of-concern SARS-COV-2] with the Delta variant was more pronounced at 108% (95% CI 78%–140%) for hospitalization, 235% (95% CI 160%–331%) for ICU admission and 133% (95% CI 54%–231%) for death.
Compared with non-VOC SARS-CoV-2 strains, the adjusted elevation in risk associated with N501Y-positive variants was 52% (95% confidence interval [CI] 42%–63%) for hospitalization, 89% (95% CI 67%–117%) for ICU admission and 51% (95% CI 30%–78%) for death.
N501Y is alpha
Immunity is always the goal if you can get it. It's not how you judge success though, you're right.
Thankfully the vaccines do drastically reduce severe illnesses though, so that's something.