The ability of this virus to spread before symptoms appear gives it quite a formidable advantage. There is no selective advantage to being less virulent on the front end of infection, because by the time symptoms appear, severe or not, the virus has already infected others.
Shorter incubation times, higher viral loads, and antigenic shifts to partially dodge neutralizing antibodies seem like traits that are being selected for, right?
My heart sank when I first learned of asymptomatic spread back in ~2/20. It’s been the worst part of trying to control this since the start, and it’s why I haven’t taken my N95 off in a 10x10 examining room yet. 😔
Thanks for dispelling wishful thinking about the virus softening. If anything it’s our T-cells making this look better… the unsung heroes as it were.
I think the biggest current issue is that our hospitals, clinics, diagnostic services, and other inpatient and outpatient healthcare facilities have dropped universal masking.
A primary prevention tool is missing.
This is putting everyone who is in need of care completely vulnerable.
We are told (dismissively) that we have the right to wear our masks...
This is irresponsible.
Many people, including me, are not completing routine tests and imaging to avoid infection.
My wonderful PCP, as well as other providers are unable to enforce masking.
Our local politicians (the Governor is an MD), but refuses to mask anywhere.
We have had local provider FB groups for 3.5 years to share and influence. But the let downs in infection prevention is a beast.
Amen sister. Life will not be going back to the way it was before the pandemic for those who don't want to get Covid, with all the known risks and long terms effects that are possible with each infection. It's super depressing, and I understand why the back-to-normal narrative is much more attractive.
Well, CDC says 97 percent of everybody has had either the virus, the vaccine, or both, and yet worldometers reports that daily American deaths have declined to single digits. So perhaps our immune systems have adapted. I’ve always been a fan of Lives of a Cell. Certain microbes are pathogenic, not because they produce toxins, but because our immune systems overreact.
There is another possibility, which is the remaining small percentage of people who have had no exposure, have avoided exposure because they have risk factors, and have isolated themselves. The article did mention their age. There’s a Wikipedia page that lists every covid related death of people famous enough to have a Wikipedia page. Almost all were old. Covid has never killed a high percentage of young people.
"To date, SARS-CoV-2 virus doesn’t appear to be on its way to becoming just another common cold virus. For the foreseeable future, the virus will continue to cause serious harm in those who are most vulnerable."
To be fair, have we ever conducted a similar study with the common cold virus--finding elderly people with no protective immunity through previous exposure and seeing how they're affected by infection? (Probably impossible to find such people, I know.) It seems that would be the only way to disentangle whether the common cold virus is inherently less pathogenic than Omicron or whether its decreased morbidity and mortality is due to widespread protective immunity, such as now exists for SARS-CoV-2 as well. Given that the vast majority of people *do* now have protective immunity against Covid via vaccination, infection, or both, who are the "most vulnerable" people who continue to be at risk of serious harm? It seems, at this point, to be the same (immunologically fragile) people who are vulnerable to influenza and common cold viruses. Is there another distinction here that I'm missing?
Unfortunately you ignore the effects of influenza on the youngest - who are immunologically naive, not fragile! And this flu season in Australia is proving particularly nasty, because there are fewer people vaccinated, and IB Victoria is proving especially serious, with 3 fatalities already - in a healthy child, a mid-teen and a 31yo father! We had an early A wave, with much higher than usual hospital presentations and admissions, but now B is increasing rapidly. Take note up North - bodes ill for you I fear in Fall and Winter!
the rates of morbidity & mortality for any infectious disease always have to be interpreted in context [prior vaccination and/or infection vs naive hosts] -- the data were presented clearly here. Bottom line Omicron variants are pathogenic, not tame
It's Not Learning Loss. It's Brain Damage, and Schools Are Letting It Happen.
More studies are showing us that children and teenagers face the same risk of Long Covid as adults. In fact, neuroscientists are especially worried about how Covid inflammation will harm brain development in children and teens. They’re still learning about it. Last year, many scientists tried to warn the public against going back to school without masks or any other protections.
So what has been achieved? For a virus which in its original form had a mortality rate a bit higher than a bad flu: We have down-regulated the innate immune system of a large % of the population (for how long, no one knows), seriously impacted our antibody system with ADE implications (potentially permanently with no proof that this can be refocuses to another configuration in time), and are betting the house on the ability of our killer cells to hold out and function on overdrive forever without braking anything else down in the process. Oh ... and no herd immunity is able to be achieved (with the current population) in light of the foregoing. And the answer is more experimental biological injectables?!
No wonder Nobel Laureate Luc Montaigner said that this is will go down on the books as one of the grossest scientific errors ever committed.
Please provide references for your assertions, preferably published papers and not websites.
Also please define what you mean by herd immunity.
Finally, a full 7% of all admissions to U.K. PICUs (paediatric intensive care units) were for children (under 16) with Covid, for the omicron variant the median age was 2 years old.
Did the Hong Kong research also account for hospitalization "for" vs. "with" COVID when determining severity for each wave? It was very clear, working in healthcare, that we had proportionately more "with" vs. "for" COVID during the Omicron wave vs. prior waves; this should be accounted for when comparing severity. Unable to view full text of the research cited.
SARS-CoV-2 (all variants) infect host cells through the spike protein binding to the ACE2 receptor.
All of the vaccines are neutralising against this part of the spike, i.e. antibodies attach to the ACE2 binding site, physically blocking the attachment to ACE2.
Other epitopes exist that may or may not be the same across variants.
Would antibodies against the SARS-CoV-2 ACE2 antigen block any ACE2 antigen that is presented on a completely different virus?
The reason I am asking is that the coronavirus that caused SARS also uses ACE2, as does one of the coronaviruses that cause the common cold.
To me, it's a like coming to the incorrect conclusion that since the late 1980s there are fewer highway deaths per capita, therefore automobile driving has improved. In point of fact, there are fewer highway deaths per capita due to seat belt laws going into effect beginning in the late 80's. I think the most important fact is that whether the subject is viruses, or highway driving, things improved.
Other researchers have shown how the spike mutations in Omicron have produced increased ability to invade cells via their TMPRSS2 receptors, while also becoming less effective at invading via a cell’s ACE2 receptors, which was the primary route for the W-1 virus to infect lung cells. This has been offered as a possible explanation for why Omicron infections have been predominantly upper respiratory, and why we are seeing greatly reduced rates of infection of lung tissues where ACE2 receptors predominate.
Here's my question: Can you say more about the HK paper? (It’s behind a paywall, so I can’t read it). Maybe the Omicron infections are manifesting different but equally consequential damage that rivals the severe damage seen in W-1 pneumonias?
I’m having trouble reconciling the Hong Kong results with the ACE2/TMPRSS2 papers. Would appreciate any light you can shed.
Fantastic study in Hong Kong. TWIV scientists (and watchers of the show) have been waiting for science instead of media guesses.
The ability of this virus to spread before symptoms appear gives it quite a formidable advantage. There is no selective advantage to being less virulent on the front end of infection, because by the time symptoms appear, severe or not, the virus has already infected others.
Shorter incubation times, higher viral loads, and antigenic shifts to partially dodge neutralizing antibodies seem like traits that are being selected for, right?
My heart sank when I first learned of asymptomatic spread back in ~2/20. It’s been the worst part of trying to control this since the start, and it’s why I haven’t taken my N95 off in a 10x10 examining room yet. 😔
Thanks for dispelling wishful thinking about the virus softening. If anything it’s our T-cells making this look better… the unsung heroes as it were.
Aloha from Hawaii.
I think the biggest current issue is that our hospitals, clinics, diagnostic services, and other inpatient and outpatient healthcare facilities have dropped universal masking.
A primary prevention tool is missing.
This is putting everyone who is in need of care completely vulnerable.
We are told (dismissively) that we have the right to wear our masks...
This is irresponsible.
Many people, including me, are not completing routine tests and imaging to avoid infection.
My wonderful PCP, as well as other providers are unable to enforce masking.
Our local politicians (the Governor is an MD), but refuses to mask anywhere.
We have had local provider FB groups for 3.5 years to share and influence. But the let downs in infection prevention is a beast.
Amen sister. Life will not be going back to the way it was before the pandemic for those who don't want to get Covid, with all the known risks and long terms effects that are possible with each infection. It's super depressing, and I understand why the back-to-normal narrative is much more attractive.
And as a former long time transplant nurse, I have strong opinions. 😷
Amen
Well, CDC says 97 percent of everybody has had either the virus, the vaccine, or both, and yet worldometers reports that daily American deaths have declined to single digits. So perhaps our immune systems have adapted. I’ve always been a fan of Lives of a Cell. Certain microbes are pathogenic, not because they produce toxins, but because our immune systems overreact.
There is another possibility, which is the remaining small percentage of people who have had no exposure, have avoided exposure because they have risk factors, and have isolated themselves. The article did mention their age. There’s a Wikipedia page that lists every covid related death of people famous enough to have a Wikipedia page. Almost all were old. Covid has never killed a high percentage of young people.
Your blog offers no scientific truth. None.
"To date, SARS-CoV-2 virus doesn’t appear to be on its way to becoming just another common cold virus. For the foreseeable future, the virus will continue to cause serious harm in those who are most vulnerable."
To be fair, have we ever conducted a similar study with the common cold virus--finding elderly people with no protective immunity through previous exposure and seeing how they're affected by infection? (Probably impossible to find such people, I know.) It seems that would be the only way to disentangle whether the common cold virus is inherently less pathogenic than Omicron or whether its decreased morbidity and mortality is due to widespread protective immunity, such as now exists for SARS-CoV-2 as well. Given that the vast majority of people *do* now have protective immunity against Covid via vaccination, infection, or both, who are the "most vulnerable" people who continue to be at risk of serious harm? It seems, at this point, to be the same (immunologically fragile) people who are vulnerable to influenza and common cold viruses. Is there another distinction here that I'm missing?
Unfortunately you ignore the effects of influenza on the youngest - who are immunologically naive, not fragile! And this flu season in Australia is proving particularly nasty, because there are fewer people vaccinated, and IB Victoria is proving especially serious, with 3 fatalities already - in a healthy child, a mid-teen and a 31yo father! We had an early A wave, with much higher than usual hospital presentations and admissions, but now B is increasing rapidly. Take note up North - bodes ill for you I fear in Fall and Winter!
the rates of morbidity & mortality for any infectious disease always have to be interpreted in context [prior vaccination and/or infection vs naive hosts] -- the data were presented clearly here. Bottom line Omicron variants are pathogenic, not tame
It's Not Learning Loss. It's Brain Damage, and Schools Are Letting It Happen.
More studies are showing us that children and teenagers face the same risk of Long Covid as adults. In fact, neuroscientists are especially worried about how Covid inflammation will harm brain development in children and teens. They’re still learning about it. Last year, many scientists tried to warn the public against going back to school without masks or any other protections.
School boards largely ignored them.
https://open.substack.com/pub/jessicawildfire/p/its-not-learning-loss-its-brain-damage?r=2jezgl&utm_medium=ios&utm_campaign=post
I've had ME/CFS for 40 years. You don't want long covid if it turns out to be even remotely similar. Some fates are worse than death.
So what has been achieved? For a virus which in its original form had a mortality rate a bit higher than a bad flu: We have down-regulated the innate immune system of a large % of the population (for how long, no one knows), seriously impacted our antibody system with ADE implications (potentially permanently with no proof that this can be refocuses to another configuration in time), and are betting the house on the ability of our killer cells to hold out and function on overdrive forever without braking anything else down in the process. Oh ... and no herd immunity is able to be achieved (with the current population) in light of the foregoing. And the answer is more experimental biological injectables?!
No wonder Nobel Laureate Luc Montaigner said that this is will go down on the books as one of the grossest scientific errors ever committed.
"Down regulated innate immunity" doesn't even make sense.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9012513/
Please provide references for your assertions, preferably published papers and not websites.
Also please define what you mean by herd immunity.
Finally, a full 7% of all admissions to U.K. PICUs (paediatric intensive care units) were for children (under 16) with Covid, for the omicron variant the median age was 2 years old.
Did the Hong Kong research also account for hospitalization "for" vs. "with" COVID when determining severity for each wave? It was very clear, working in healthcare, that we had proportionately more "with" vs. "for" COVID during the Omicron wave vs. prior waves; this should be accounted for when comparing severity. Unable to view full text of the research cited.
SARS-CoV-2 (all variants) infect host cells through the spike protein binding to the ACE2 receptor.
All of the vaccines are neutralising against this part of the spike, i.e. antibodies attach to the ACE2 binding site, physically blocking the attachment to ACE2.
Other epitopes exist that may or may not be the same across variants.
Would antibodies against the SARS-CoV-2 ACE2 antigen block any ACE2 antigen that is presented on a completely different virus?
The reason I am asking is that the coronavirus that caused SARS also uses ACE2, as does one of the coronaviruses that cause the common cold.
Amazing you don’t mention the gain of function research that went into making his virus so infectious though only deadly to older people.
Only deadly to older people? All age groups have been affected. True that over 65 is more vulnerable but that's true for all ARDS.
Thank you Dr Offit.
For papers, articles, studies, etc. I would refer you to the three section blog on the website voiceforscienceandsolidarity.org. In respect to herd immunity, I view it as achieved when a contextually relevant a critical mass of the population achieves sterilizing immunity. A difusión opinion piece of interest on the topic: www.statnews.com/2022/03/25/how-we-got-herd-immunity-wrong/. Lastly, for snippets of what Luc Montaigner’s thoughts on variants, a video: https://odysee.com/@Belfasteye.com:9/-Luc-Montagnier2:2.
Is it plausible that what appears to be the virus weakening is an inscrutable combination of
- Virus attenuating
- Increasing immunity in the population
and
- (tragically) host evolution
To me, it's a like coming to the incorrect conclusion that since the late 1980s there are fewer highway deaths per capita, therefore automobile driving has improved. In point of fact, there are fewer highway deaths per capita due to seat belt laws going into effect beginning in the late 80's. I think the most important fact is that whether the subject is viruses, or highway driving, things improved.
Betteridge's Law of Headlines strikes again.
Other researchers have shown how the spike mutations in Omicron have produced increased ability to invade cells via their TMPRSS2 receptors, while also becoming less effective at invading via a cell’s ACE2 receptors, which was the primary route for the W-1 virus to infect lung cells. This has been offered as a possible explanation for why Omicron infections have been predominantly upper respiratory, and why we are seeing greatly reduced rates of infection of lung tissues where ACE2 receptors predominate.
Here's my question: Can you say more about the HK paper? (It’s behind a paywall, so I can’t read it). Maybe the Omicron infections are manifesting different but equally consequential damage that rivals the severe damage seen in W-1 pneumonias?
I’m having trouble reconciling the Hong Kong results with the ACE2/TMPRSS2 papers. Would appreciate any light you can shed.