17 ms·

> There are evolutionary pressures on viruses that tend to weaken them over time. Those evolutionary pressures relate to transmissibility. Basically, a virus t

by wrl 5y ago

> There are evolutionary pressures on viruses that tend to weaken them over time. Those evolutionary pressures relate to transmissibility. Basically, a virus that kills its host before it can spread doesn't spread very far at all. SARS-CoV-2's defining feature of asymptomatic spread decouples this and so far hasn't led to weakening – indeed, Delta is both substantially more transmissible and more likely to cause severe disease and death.

jdavis703 5y ago
Right, and because of severe disease and death health authorities introduced more stringent rules to reduce transmission. Evolutionary this should eventually pressure the virus in to becoming less severe (assuming public health policy continues to be focused on preventing severe disease and death).
- VortexDream 5y ago
  This assumes a uniform global response. Not even the US can get their pandemic under control. There are so many breeding grounds across the world where Covid is completely free to mutate that it doesn't matter if a handful of countries have it figured out. You also have an increasing pushback against measures even in European countries with high vaccination rates. If a high impact variant emerges, it's going to become harder and harder on a political (and even economic) level to contain it.
  - adventured 5y ago
    > Not even the US can get their pandemic under control. That's because the vaccines don't effectively stop the spread of SARS2. This is one of the great lies still being shoveled on the public - despite the facts that prove otherwise. See: Britain has a lot more cases per capita than the US, despite their high vaccination rates and more aggressive lock-down & restrictive measures taken. Or see: the New England states with high vaccination rates and a recent record surge in cases. Or see: Israel's recent epic case surge despite their very high vaccination rate. The vaccines dramatically reduce mortality and that's the primary reason most people should get the jab. There's zero evidence so far that we can actually stop SARS2 via vaccine. It doesn't make sense to be forced to live in bomb shelters forever as eg Australia is doing, that's idiotic and tyrannical. What matters isn't the case counts, it's the number of deaths that matter and Britain's high vaccination rate is doing its job there for example.
    - ekidd 5y ago
      > Or see: the New England states with high vaccination rates and a recent record surge in cases. As a resident of New England, I've been expecting a fall surge for a while. In the north, we're all shutting windows and turning on our furnaces at night, which means much worse ventilation. The afternoons are still warm enough to socialize outside, but that will start to change in November. Followed by holiday travel. And we still have towns with low vaccination rates. Our absolute numbers are still fairly low in many places, and we don't have people lined up in the corridors of the local hospitals. > What matters isn't the case counts, it's the number of deaths that matter I actually think that severe illness counts are important, too. I'll make some sacrifices to avoid hospitalization or merely being incapacitated for a couple weeks.
  - hanselot 5y ago
    > Not even the US can get their pandemic under control. That's because the vaccines don't effectively stop the spread of SARS2. This is one of the great lies still being shoveled on the public - despite the facts that prove otherwise. See: Britain has a lot more cases per capita than the US, despite their high vaccination rates and more aggressive lock-down & restrictive measures taken. Or see: the New England states with high vaccination rates and a recent record surge in cases. Or see: Israel's recent epic case surge despite their very high vaccination rate. The vaccines dramatically reduce mortality and that's the primary reason most people should get the jab. There's zero evidence so far that we can actually stop SARS2 via vaccine. It doesn't make sense to be forced to live in bomb shelters forever as eg Australia is doing, that's idiotic and tyrannical. What matters isn't the case counts, it's the number of deaths that matter and Britain's high vaccination rate is doing its job there for example. See India, where prior to introduction of vaccines they were effectively countering the disease. See Sweden, where prior to introduction of vaccines they were effectively countering the disease. See any country where vaccine rates are high, mortality rate soon skyrockets. If you need sources to read data that is available EVERYWHERE you are the problem, and you should take the vaccine, because at least that means in 6months to 3 years you won't be a problem anymore. I have no issue with you taking a vaccine to gain immunity from a disease. But you can't force me to be a part of your experiment. If your vaccine worked, why would I need to take it? Surely it would be me that should be worried, yet here I am, alive, and not infected.
lamontcg 5y ago
The need to achieve immune escape can also pressure the virus to evolve antigenically which can promote transmissibility through escape, while impairing ACE2 binding or endocytosis compared to currently circulating variants. So if the ancestral strain + variants all cannot spread epidemically any more due to the build up of immunity in the population, then a strain which achieves immune escape and an R0 of > 1.0 would be favored even though the virus might be much less "fit" and less virulent in a totally naive population. Clearly though the major adaptation is going to be on the human side with most of the population eventually acquiring T-cells, which will greatly decrease the virulence going forwards.
- 75dvtwin 5y ago
  > while impairing ACE2 binding It appears that COVID-19 can also enter cells (these would be immune cells that came to 'help') via so called Fc-pathway. Therefore allow the virus to multiply even more "... In addition to viral entry via ACE2, antibodies against coronavirus spike proteins (anti-spike-S-IgG) can induce antibody-dependent enhancement (ADE) of viral entry via type II Fcγ receptors. ..." [1] [1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406916/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406916/
  - lamontcg 5y ago
    That really has nothing to do with what I wrote, other than for you to write about ADE, which is not a practical issue for anyone to worry about with SARS-CoV-2: https://www.science.org/content/blog-post/new-antibody-dependent-enhancement-hypothesis https://www.science.org/content/blog-post/new-antibody-depen... I can't flag you, but someone else really should since your followup is completely disingenuous.
    - 75dvtwin 5y ago
      sorry, but your assessment of what is genuine vs disingenuous, is very disingenuous in itself. Perhaps, it is time to relinquish the presumptions of moral superiority -- and just discuss technical details without the drama ... I am saying that you wrote does not cover full spectrum of how the virus replicates, therefore your comment does illuminate the complexity that's present in interaction with our immune system. Which includes, according to the NIH paper I referenced, antibody-dependent-enhancement (ADE).
mariodiana 5y ago
Which is what makes what happened with Marek's disease so interesting.
brigandish 5y ago
Presymptomatic might be a better term than asymptomatic, as the evidence for asymptomatic spread is weak and weakening. One example[1]: > Research early in the pandemic suggested that the rate of asymptomatic infections could be as high as 81%. But a meta-analysis published last month, which included 13 studies involving 21,708 people, calculated the rate of asymptomatic presentation to be 17%. The analysis defined asymptomatic people as those who showed none of the key COVID-19 symptoms during the entire follow-up period, and the authors included only studies that followed participants for at least seven days. There are many more I've read where the authors have tried to quantify asymptomatic spread and been found wanting (studies on children are particularly enlightening). I wouldn't be surprised if the final figure ends up being very close to, if not, zero, though we're still in the clutches of the initial panic so I suspect those findings to take time due more to social resistance than the frictions involved in actual science. [1] https://www.nature.com/articles/d41586-020-03141-3?error=cookies_not_supported&code=00c272c7-916e-422f-9bdb-165fcc862b7b https://www.nature.com/articles/d41586-020-03141-3?error=coo...
- wrl 5y ago
  Note that I said "asymptomatic spread", not "asymptomatic infection" – i.e. a host spreading SARS-CoV-2 without experiencing or showing symptoms from the active infection. Whether the host goes on to experience symptoms from said infection at some point in the future isn't what I was referring to.
  - brigandish 5y ago
    Right, and that changes nothing about my response as that's what I was responding to, there is still weak and weakening evidence for transmission by those with asymptomatic infection. For example[1]: > We determined secondary attack rates (SAR) among close contacts of 59 asymptomatic and symptomatic coronavirus disease case-patients by presymptomatic and symptomatic exposure. We observed no transmission from asymptomatic case-patients and highest SAR through presymptomatic exposure. [1] https://wwwnc.cdc.gov/eid/article/27/4/20-4576_article https://wwwnc.cdc.gov/eid/article/27/4/20-4576_article

by wrl 5y ago

jdavis703 5y ago

Right, and because of severe disease and death health authorities introduced more stringent rules to reduce transmission. Evolutionary this should eventually pressure the virus in to becoming less severe (assuming public health policy continues to be focused on preventing severe disease and death).

VortexDream 5y ago
This assumes a uniform global response. Not even the US can get their pandemic under control. There are so many breeding grounds across the world where Covid is completely free to mutate that it doesn't matter if a handful of countries have it figured out. You also have an increasing pushback against measures even in European countries with high vaccination rates. If a high impact variant emerges, it's going to become harder and harder on a political (and even economic) level to contain it.
- adventured 5y ago
  > Not even the US can get their pandemic under control. That's because the vaccines don't effectively stop the spread of SARS2. This is one of the great lies still being shoveled on the public - despite the facts that prove otherwise. See: Britain has a lot more cases per capita than the US, despite their high vaccination rates and more aggressive lock-down & restrictive measures taken. Or see: the New England states with high vaccination rates and a recent record surge in cases. Or see: Israel's recent epic case surge despite their very high vaccination rate. The vaccines dramatically reduce mortality and that's the primary reason most people should get the jab. There's zero evidence so far that we can actually stop SARS2 via vaccine. It doesn't make sense to be forced to live in bomb shelters forever as eg Australia is doing, that's idiotic and tyrannical. What matters isn't the case counts, it's the number of deaths that matter and Britain's high vaccination rate is doing its job there for example.
  - ekidd 5y ago
    > Or see: the New England states with high vaccination rates and a recent record surge in cases. As a resident of New England, I've been expecting a fall surge for a while. In the north, we're all shutting windows and turning on our furnaces at night, which means much worse ventilation. The afternoons are still warm enough to socialize outside, but that will start to change in November. Followed by holiday travel. And we still have towns with low vaccination rates. Our absolute numbers are still fairly low in many places, and we don't have people lined up in the corridors of the local hospitals. > What matters isn't the case counts, it's the number of deaths that matter I actually think that severe illness counts are important, too. I'll make some sacrifices to avoid hospitalization or merely being incapacitated for a couple weeks.
- hanselot 5y ago
  > Not even the US can get their pandemic under control. That's because the vaccines don't effectively stop the spread of SARS2. This is one of the great lies still being shoveled on the public - despite the facts that prove otherwise. See: Britain has a lot more cases per capita than the US, despite their high vaccination rates and more aggressive lock-down & restrictive measures taken. Or see: the New England states with high vaccination rates and a recent record surge in cases. Or see: Israel's recent epic case surge despite their very high vaccination rate. The vaccines dramatically reduce mortality and that's the primary reason most people should get the jab. There's zero evidence so far that we can actually stop SARS2 via vaccine. It doesn't make sense to be forced to live in bomb shelters forever as eg Australia is doing, that's idiotic and tyrannical. What matters isn't the case counts, it's the number of deaths that matter and Britain's high vaccination rate is doing its job there for example. See India, where prior to introduction of vaccines they were effectively countering the disease. See Sweden, where prior to introduction of vaccines they were effectively countering the disease. See any country where vaccine rates are high, mortality rate soon skyrockets. If you need sources to read data that is available EVERYWHERE you are the problem, and you should take the vaccine, because at least that means in 6months to 3 years you won't be a problem anymore. I have no issue with you taking a vaccine to gain immunity from a disease. But you can't force me to be a part of your experiment. If your vaccine worked, why would I need to take it? Surely it would be me that should be worried, yet here I am, alive, and not infected.

lamontcg 5y ago

The need to achieve immune escape can also pressure the virus to evolve antigenically which can promote transmissibility through escape, while impairing ACE2 binding or endocytosis compared to currently circulating variants. So if the ancestral strain + variants all cannot spread epidemically any more due to the build up of immunity in the population, then a strain which achieves immune escape and an R0 of > 1.0 would be favored even though the virus might be much less "fit" and less virulent in a totally naive population. Clearly though the major adaptation is going to be on the human side with most of the population eventually acquiring T-cells, which will greatly decrease the virulence going forwards.

75dvtwin 5y ago
> while impairing ACE2 binding It appears that COVID-19 can also enter cells (these would be immune cells that came to 'help') via so called Fc-pathway. Therefore allow the virus to multiply even more "... In addition to viral entry via ACE2, antibodies against coronavirus spike proteins (anti-spike-S-IgG) can induce antibody-dependent enhancement (ADE) of viral entry via type II Fcγ receptors. ..." [1] [1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406916/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406916/
- lamontcg 5y ago
  That really has nothing to do with what I wrote, other than for you to write about ADE, which is not a practical issue for anyone to worry about with SARS-CoV-2: https://www.science.org/content/blog-post/new-antibody-dependent-enhancement-hypothesis https://www.science.org/content/blog-post/new-antibody-depen... I can't flag you, but someone else really should since your followup is completely disingenuous.
  - 75dvtwin 5y ago
    sorry, but your assessment of what is genuine vs disingenuous, is very disingenuous in itself. Perhaps, it is time to relinquish the presumptions of moral superiority -- and just discuss technical details without the drama ... I am saying that you wrote does not cover full spectrum of how the virus replicates, therefore your comment does illuminate the complexity that's present in interaction with our immune system. Which includes, according to the NIH paper I referenced, antibody-dependent-enhancement (ADE).

mariodiana 5y ago

Which is what makes what happened with Marek's disease so interesting.

brigandish 5y ago

Presymptomatic might be a better term than asymptomatic, as the evidence for asymptomatic spread is weak and weakening. One example[1]: > Research early in the pandemic suggested that the rate of asymptomatic infections could be as high as 81%. But a meta-analysis published last month, which included 13 studies involving 21,708 people, calculated the rate of asymptomatic presentation to be 17%. The analysis defined asymptomatic people as those who showed none of the key COVID-19 symptoms during the entire follow-up period, and the authors included only studies that followed participants for at least seven days. There are many more I've read where the authors have tried to quantify asymptomatic spread and been found wanting (studies on children are particularly enlightening). I wouldn't be surprised if the final figure ends up being very close to, if not, zero, though we're still in the clutches of the initial panic so I suspect those findings to take time due more to social resistance than the frictions involved in actual science. [1] https://www.nature.com/articles/d41586-020-03141-3?error=cookies_not_supported&code=00c272c7-916e-422f-9bdb-165fcc862b7b https://www.nature.com/articles/d41586-020-03141-3?error=coo...

wrl 5y ago
Note that I said "asymptomatic spread", not "asymptomatic infection" – i.e. a host spreading SARS-CoV-2 without experiencing or showing symptoms from the active infection. Whether the host goes on to experience symptoms from said infection at some point in the future isn't what I was referring to.
- brigandish 5y ago
  Right, and that changes nothing about my response as that's what I was responding to, there is still weak and weakening evidence for transmission by those with asymptomatic infection. For example[1]: > We determined secondary attack rates (SAR) among close contacts of 59 asymptomatic and symptomatic coronavirus disease case-patients by presymptomatic and symptomatic exposure. We observed no transmission from asymptomatic case-patients and highest SAR through presymptomatic exposure. [1] https://wwwnc.cdc.gov/eid/article/27/4/20-4576_article https://wwwnc.cdc.gov/eid/article/27/4/20-4576_article