For those expecting herd immunity: this study kinda buries that possibility.

https://www.bing.com/search?q=covid+infections+up+deaths+down&search=&form=QBLH

 

I feel it’s important to add a little to post#75 above.

To be clear, antigenic drift occurs in most viruses to some extent. There are a lot of variables that determine how much occurs in each type species. In influenza viruses, antigenic drift happens quickly and is a huge factor in immunity and vaccine production. In rhinovirus, antigenic drift is typically so low it is irrelevant to vaccine production.

 

Tetanus used to be a yearly shot, than went to 5 years and is now 10 years.

 

You can be sure that the infection rates in our country are much higher than the official statistics.

But why are you comparing us with third world countries? Is that how low the bar has come with Trump? We have the worst response in the world because we have the resources, but the response wasn't there. This administration mishandled this pandemic badly.

In February, we were the most prepared country in the world for a pandemic, according to the World Security Health Index. Today you are desperately looking for some third world country so we can whine about how unfair it is to say that they are beating our ass in their response.

That would be inaccurate. Mexico had a very poor response to the virus. But they had their worst numbers in June and have now taken the obvious rational measures: shut downs, mandatory masks, mandatory social distancing, ... We probably have yet to see our worst numbers, given that measures have been limited to some cities or counties, and some of our states that are doing the worst are still mandating school openings.... Idiotic!

 

Why are there too many existing strains? Where did they come from? What caused them to be different?

"Changing strains"????

Oh God. My suspicions have been confirmed. You believe that the way "mutations" occur is like when Turtles fall in a radioactive pond and "change" into intelligent beings with superpowers.

This is hilarious!

 

Predominantly recombination.

Yes. Because mutations are only a small part of why many viruses drift and shift over time. Recombination is key to the antigenic diversity of rhinovirus, not mutations. So we use the word “change” to describe the totality of all these different metrics. Of course you were unaware of recombination so you made another error.

Yes, your descent into ad hominem again is hilarious when you can’t present any facts. It’s good you are laughing at yourself along with the rest of PF.

Since I’ve never had television I’m only aware of the Turtles by way of references to them like you’ve used. If you want me to gain some insight from them you will have to fill me in. It sounds like a kid thing, if I remember right I think a couple kids at school talked about it back in the day. If that’s the case, at that age I was probably reading up on pathogens that affect reptiles to try and figure out why my pet box turtle died instead of watching TV. That probably explains why you don’t know anything about viruses, immunity, or vaccines and I’m educating you on those subjects while your expertise seems to be in TV shows.

You are a glutton for punishment.

 

No, that's how it's always been in the US.
Progressives have always tried to compare the US to other First World countries to try to say "what a terrible job" America is doing. But they're only comparing the US to other White English-speaking countries, Western Europe, and a small handful of East Asian countries. Sort of cherry picking.

 

Bzzzzzz! Wrong answer!

Do you want to try again?

I repeat: what produced all those "too many existing strains" you mentioned?

This is an "Open Book" test. You can use research. In fact, I strongly suggest that you do.

If you can't answer that one try this one:

Draw a clock at five after ten.

 

Not really. We used to be a first world country. You might not remember this because that was waaaay back before Trump turned us into a Banana Republic. Worse! Because we don't even produce bananas.

 

Remember the first link I posted on this subject? It mentioned a vaccine would need to cover about 80 strains. Well, of those 80 strains currently we have evidence about 46 are the result of recombination. A few years ago we thought only 23 were recombinant. As our methods improve and we map more unknowns that percentage of recombinants will likely increase. The “C” species is rife with recombinant strains and it is the most recently discovered species so as we map and test the new “C” strains the percentage of recombinant will increase as well. So we have now learned that recombination is indeed predominantly responsible for the antigenic diversity of rhinovirus relevant to common colds.

Furthermore, mutation rates are decoupled from antigenic drift. This is demonstrated by comparing rhinovirus with influenza. The mutation rate of rhinovirus is higher than that of influenza. Yet antigenic drift of rhinovirus is much less, as demonstrated by my first link and pull quote.

Finally, the idea mutation rate or antigenic drift are the reason we don’t have a cold vaccine is not logical. You actually didn’t use correct terminology but you said this:

This is completely illogical because influenza has a much “faster” antigenic drift than rhinovirus. In your layman terminology influenza vaccines “stop working” much sooner than rhinovirus ones. In fact influenza “stops working” in months. Rhinovirus vaccines are still “working” decades after development. Yet we have a new influenza vaccine every year! How can this be? Because we figured out how make vaccines for a handful of viral strains with influenza but haven’t yet figured out how to cover 80 strains with one vaccine for the common cold. Just like my links say!

 

If a vaccine can cover 46 of 80 strains that differentiated through recombination, that means recombination is not nearly what accounts for all those "too many existing strains" that have kept us from finding a vaccine that covers all, which is what the poster wanted to know.

Therefore, what does account for them is.... all together now.... Mutation!

The rest of your copy-paste is irrelevant to the question the poster asked. But thanks for sharing anyway.

 

You’ve been shown to be incorrect.

Your initial claim is:

It is a fact vaccines for the cold do not stop working. They are effective decades after development. There is no comprehensive vaccine for the cold because there are too many strains in circulation. The strains in circulation are predominantly the product of recombination.

All the above I’ve documented. You have again denied science. Recombination is real, whether you want to accept it or not. And recombination is not mutation. LOL

Thanks for letting me demonstrate your lack of knowledge and your denial of science again. Till next time...and with your record of making a false statement on biology at least daily it won’t be long...take care.

Oh, and you have again made claims with no foundation in science. Bad habit you have.

 

Anybody who has received it and still gets the cold would beg to differ.

 

Let’s stick to reality. I know it’s hard for you because realities of the natural world conflict with your opinions, but I’m only interested in facts.

 

There is no way to eradicate the common cold because there are too many viruses that cause it. The coronavirus family is responsible for only 20% of the common colds out there, but 80% of other cases are by other viruses, with 30% of them not even having been named yet and counting in the hundreds. It doesn't mean that this one specific SARS-CoV-2 can not be eradicated. The task of doing it would be much less complex than the rather impossible task of eradicating the common cold. Remember, the first SARS did die out.

This said, I agree with you that it is highly unlikely, given how wide-spread it is, now. But it is not as unlikely as being able to get rid of the common cold.

The SARS-CoV-2 will probably be endemic or will make a seasonal comeback. But if it doesn't mutate too much, and it hasn't so far, it is possible that we'll have vaccines that will have decent efficacy. The current threshold for efficacy approval is 50%. If we get a vaccine that is, say, 70% effective, we'd need to vaccinate 71% of the population (given a R0 of 2.0) to interrupt completely the chain of transmission. I know that achieving 70% is not easy. The flu shot is only taken by 50% of Americans, and our political climate, so divided, is not conducive of 70% of the population accepting the vaccine.

We'll see. First things first. We need to get a safe and effective vaccine, first. I'm actually optimistic that we will.

 

Not necessarily. Despite this study I still have high hopes for vaccines.

This study is not as discouraging as it seems, because there is still B-cell and T-cell immunity. Even after antibodies fade away, an individual who has had the infection or has had an effective vaccine (if a safe and effective one is developed and passes phases 1, 2, and 3 trials), if he/she encounters the virus again, the virus may start by multiplying given that the antibodies are gone, but cell immunity will kick in and rapidly produce more antibodies and T cells will kill infected cells as well, and the person will have an asymptomatic or very mild disease that will be short-lived.

This study has implications for whether or not we'll be able to ever achieve herd immunity, with or without vaccination (because for herd immunity neutralizing antibodies need to be active in a significant proportion of the population; at least 50% for a virus with a R0 of 2.0), but it doesn't mean that a person who has had the disease or a good vaccine will be entirely unprotected once the antibodies are gone.

 

So basically, this is going to be the new influenzia moving forward?

 

You may want to buy a flame suit if you are going to be bandying numbers like 50% for herd immunity around. Very taboo here.

 

Thanks for the heads up, but it's just a fact. There is a way to calculate herd immunity:

https://plus.maths.org/content/maths-minute-r0-and-herd-immunity

For an R naught of 2.0, it comes up to 50%.

On the other hand, this paper supposes that 2.5 is the higher end of the estimates for COVID-19, which is not true. The higher end is 5.7, which gives us a herd immunity threshold of 82.5%.

The effective R naught number however should not be understood as an absolute number. It varies with the conditions. It can be higher in a crowded place with no social distancing, no masks, no nothing. In an epicenter in São Paulo, Brazil, it's been measured as high as 18, which is huge, and measles-like.

But for regular epidemiological conditions, an estimate of 2.0 to 2.5 is probably accurate so we'd need a threshold of about 50% to 60%.

You know, these things are not *opinion*, they are *science* and they've been well studied, and well established.

So if someone wants to burn me at the stake because I'm saying so, I can take it. I'm a grown boy. I deal in scientific facts, not opinion.

 

It's possible. We'll see. Remember, this is a novel coronavirus. It's been around for 8 months. The flu in some estimates is supposed to having been around for 3,000+ years. So we don't entirely know the behavior of this virus, yet.

 

Oh, and I should add this:

This said, the calculation of the Herd Immunity Threshold based on the R0 number involves a percentage of the *susceptible* population, so there is some leeway in this, as we don't know very well yet the issue of who is susceptible, who is not. For example, a certain blood type may make people less susceptible. There's been some evidence of people with some partial immunity against the SARS-CoV-2, presumably due to previous contact with other coronaviruses. There's been speculation that factors such as level of vitamin D, level of zinc, chronic use of Pepcid, certain hormonal states, etc., might make people less susceptible. None of these factors are confirmed; more research is needed, but there's been some interesting trends that have been suggested.

So presumably, the herd immunity threshold for the population as a whole might be less impressive than the one calculated on bases of a R0 number estimated while the virus was collecting the low-hanging fruit of the more susceptible population.

I doubt it, though. This virus is very infectious, so I expect a high Herd Immunity Threshold, but in a novel disease like this one, data are incomplete and premature so the jury is still out.

 

It will be nice to have you around. People who prefer “science” over media spin and confirmation bias are in short supply here.

On herd immunity I’ve been advocating for including heterogeneity of populations in the equation for weeks now. I broached it again yesterday and posted this.

As evidence accumulates, I propose effective herd immunity will occur somewhere around or below 50%. You have mentioned most of the reasons I’ve come to that conclusion. Vitamin D is s good call. I need to look up a claim I heard the other day that the American public had become quite deficient in vit D.

Anyway, welcome to the forum.

 

Thanks. I'm glad to see a poster who knows what he/she is saying and who quotes scientific papers rather than media articles. Yesterday I posted in a thread here, where the OP had quoted a Fox Business report about a paper published by the CDC on July 16th, and the article grossly misunderstood the paper, supposing that it supports that people are more likely to get the infection at home than in the community. I went to the paper itself to explore it, and the data support a totally different conclusion than what the Fox Business journalist supposed (either naively or maliciously).

Anyway, I hear you about New York and the lack of a second wave as indication of some herd immunity, but I was taken aback by another paper published this week - I'll see if I can get the link for you later - with serology survey of various cities, and in NYC the percentage of antibodies in the population was only 6.8% (still the highest among the surveyed ones; SanFran the lowest with 1%). It's true that some serology surveys have suffered from huge methodology flaws, like the Santa Clara one that used a faulty antibody test and got a non-random, biased sample. I read this paper very rapidly and didn't explore enough the methodology to see if it is sound. Anyway, for what it's worth.

Cheers.