We've been sequencing the crap out of this virus. If it's mutated to a less virulent strain we will pick that up quickly.

I'm guessing Drs are just getting better at keeping people alive.

Either way, lower death rates are good news.

amercer said:

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We've been sequencing the crap out of this virus. If it's mutated to a less virulent strain we will pick that up quickly.

I'm guessing Drs are just getting better at keeping people alive.

Either way, lower death rates are good news.

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This. Let's not forget to give credit where credit is due to the amazing doctors who are learning in the trenches as they go.

amercer said:

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We've been sequencing the crap out of this virus. If it's mutated to a less virulent strain we will pick that up quickly.

I'm guessing Drs are just getting better at keeping people alive.

Either way, lower death rates are good news.

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The doctors quoted were talking about a quantitatively smaller viral load. That's not a treatment difference, that's something else.

The virus is not mutating fast enough to weaken substantially in this amount of time.

Will it eventually weaken? Yes, it is expected that it will. However, this will be expected over many years and decades.

The idea that infections today are not as serious as infections in February or March probably has more to do with other factors than the genetics of the virus.

More likely scenario is that the virus is now making it into sub-populations that exhibit some form of natural general immunity/tolerance that minimizes the impact of coronavirus.

We see this occur during every other natural selection event on the planet and across all species it would only make sense here as well. It was always likely we had a reservoir of highly immune genetic populations.

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The virus is not mutating fast enough to weaken substantially in this amount of time.

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This is the type of stuff that makes me frustrated. How these f'@k would anyone know this? Are you God? We should defer to the qualified research and not throw down unqualified absolutes.

We have sequenced this virus now and its isolates tens of thousands of times with the genome sequence freely available to anyone to download it and look at it yourself.

From that, we can easy calculate the mutation rate and observe the mutations, their locations, and whether they may have any particular function or are just silent mutations.

That is deferring to the 'qualified' research.

Ranger222 said:

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The virus is not mutating fast enough to weaken substantially in this amount of time.

Will it eventually weaken? Yes, it is expected that it will. However, this will be expected over many years and decades.

The idea that infections today are not as serious as infections in February or March probably has more to do with other factors than the genetics of the virus.

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The virus mutates about every second transmission. It actually doesn't take much to weaken the virus, but they have to be in specific locations. This isn't a "fast enough" thing, it is a pure random chance thing. Faster mutating means more chances to roll the dice and hope for a winning number, but you can roll a winning number on the first try too.

For instance.....

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May 6, 2020 / By Talia Kaplan | Fox News

Dr. Ramin Oskoui, a cardiologist and CEO of Foxhall Cardiology, reacted on Tuesday to a study that found a new coronavirus mutation reportedly mirrors a change that occurred as the SARS virus began to weaken, saying, "it's well-known that as viruses progress, they typically mutate to weaker forms."

"The phenomenon is known as 'Muller's Ratchet,'" Oskoui told "The Ingraham Angle"

He added that this is "virology 101."

"This is how they go away. They typically mutate, as well as herd immunity, to attenuate weaker strains that no longer make people so ill," Oskoui continued.

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https://orthospinenews.com/2020/05/06/doctors-react-to-study-revealing-covid-19-mutations-may-be-weakening-this-is-virology-101/

Now I realize that is Fox News and I should keep my bag of salt ready bu I would hope that the guy quoted has better training and research experience than most of the Holiday Inn Express types.

I'm not sure there is any scientific information to make the statement "it actually doesn't take much to weaken the virus". If so, please provide sources.

You are right its random chance and role of the dice. But you and I both know that the likelihood of hitting he right dice roll is low percentage. Far harder than you are implying. It will take thousands of random mutations and we are just not there yet.

We are also completely skipping over the idea and process whether said mutation that weakens the virus would actually confer fitness to the virus that would allow it to outcompete other circulating non-mutated isolates, and the amount of time it would take for such an isolate to become dominant in infections.

So far there are only a couple of examples of large mutations found within the viral genome -- a group sequenced in Singapore and another in Arizona. To my knowledge, both have been only found locally with no spread outside their geographic regions.

Again, the idea that the virus is "weakening" has more to do with how WE are behaving in terms of response, treatments and effective social distancing measures rather than anything with viral genetics. It is not helpful to put out the idea to the public that the virus is weakening because it will only cause people to not follow social distancing protocols.

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We have sequenced this virus now and its isolates tens of thousands of times with the genome sequence freely available to anyone to download it and look at it yourself.

From that, we can easy calculate the mutation rate and observe the mutations, their locations, and whether they may have any particular function or are just silent mutations.

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This is the same line served up for the "It can't have arrived before XYZ date" discussion. When you actually read most commentary, the folks doing the research were happy to admit that new information merited new findings and folks are still trying to figure this thing out.

I keep seeing this " We can easily...." Can you? I rarely see this degree of certainty in most any field.

As I said in my original post, this is true but we are almost certainly not dealing with a weakened isolate right now. It WILL weaken but on a longer evolutionary time scale, not in four months.

I guess a more direct question... and I will shut up. And go away if so...... do you actually work in the genetic research firkd or are you just expressing strongly stated gut feelings based on internet research?

I have a PhD in Microbiology/Immunology and I currently am working on a SARS-CoV-2 project.

That might have been the best 3 post exchange in the history of TexAgs.

Ranger222 said:

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I'm not sure there is any scientific information to make the statement "it actually doesn't take much to weaken the virus". If so, please provide sources.

You are right its random chance and role of the dice. But you and I both know that the likelihood of hitting he right dice roll is low percentage. Far harder than you are implying. It will take thousands of random mutations and we are just not there yet.

We are also completely skipping over the idea and process whether said mutation that weakens the virus would actually confer fitness to the virus that would allow it to outcompete other circulating non-mutated isolates, and the amount of time it would take for such an isolate to become dominant in infections.

So far there are only a couple of examples of large mutations found within the viral genome -- a group sequenced in Singapore and another in Arizona. To my knowledge, both have been only found locally with no spread outside their geographic regions.

Again, the idea that the virus is "weakening" has more to do with how WE are behaving in terms of response, treatments and effective social distancing measures rather than anything with viral genetics. It is not helpful to put out the idea to the public that the virus is weakening because it will only cause people to not follow social distancing protocols.

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Oh come on. You know as well as I do that a single mutation can drastically effect the function of a protein just like other mutations can have no effect. The Az group linked above with the 81bp deletion, for example. You also know that it doesn't take a large mutation to do that. A frame shift mutation could wreak a protein or a point mutation to change a codon to a stop codon. And altering a single critical amino acid could reduce the function sufficiently to slow the viral replication down. You also know that just staring at a genome sequence isn't going to tell you if this one point mutation that caused this one amino acid change had a significant effect or no change at all. We could make some pretty good guesses by mapping the amino acid sequence to a homologous structure, but that is about it.

You also don't need to accumulate thousands of random mutations in a single virus to weaken it. There are probably dozens, maybe hundreds of possible single point mutations that would weaken the virus. And yeah, in a genome of 30000, the probability of hitting on one of those is low. But with hundreds of thousands of infected individuals, it is possible we have hit on one or more of those already.

To the larger point, yeah a global decrease in IFR isn't the result of some weaker virus that showed up in Italy or Az, but that has more to do with how viruses spread than if a weakening mutation has happened.

So, it isn't So much that the virus isn't mutating fast enough, it is that there hasn't been sufficient time for weaker mutants to outcompete the worse ones on a global (and probably not even on a regional) scale.

culdeus said:

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Does world travel make mutations more or less likely? In another way, are mutations caused by in breeding more or less?

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No. Viruses don't reproduce sexually. The viral mutations are caused by mistakes in copying the virus in the host.

My curiosity is piqued by the idea of a quantitatively smaller viral load. The Italian doc is quoted as saying they are seeing infinitesimally smaller viral loads the last 10 days than during their peak. This isn't some random doc but is the head of one of the largest research hospitals in Europe, so I think we can assume he's not talking out his rear.

The topic of "viral load" and how it impacts spread, and especially severity, has been discussed over the last few months but I don't know that there has really been much clarity let alone anything approaching a consensus.

This raises a lot of questions which aren't necessarily about the virus possibly mutating, but more about how this virus actually works in its "original" state.

Why are they seeing such a huge difference in viral load?

How much does viral load impact symptomatic vs asymptomatic infection?

How much does it impact severity of symptoms?

If a patient has "infinitesimally smaller" viral load, is that enough to trigger antibodies/immunity or is there a threshold which must be met to trigger immune response?

You can see how critical some of these questions and answers are:

If a tiny viral load leads to asymptomatic patients but yields immunity, then we already have a poor man's vaccine.

Even if we can't go that far, it's still important in determining ongoing mitigation strategies.