COVID-19 - On the Ground

[PhDhawk]

PhD: have you seen this?



Back in the spring of last year, a 45-year-old man went to the Brigham and Women's Hospital in Boston because of a coronavirus infection. Doctors treated him with steroids and discharged him five days later.

But the infection never went away — for 154 days. "He was readmitted to the hospital several times over the subsequent five months for recurrence of his COVID-19 infection and severe pneumonia," says infectious disease doctor Jonathan Li at Harvard Medical School, who helped treat the man.

"So this is an extraordinary individual," Li says.

So extraordinary in fact that this man's case is offering scientists surprising clues about where the new coronavirus variants emerged and why they're causing explosive outbreaks on three continents.

To be clear here, the man wasn't what doctors call a "long hauler," or a person who clears a coronavirus infection and then continues to have health problems for months. This man had living, growing virus in his body for five months, Li says. The same infection lasted for five months.

"That is one of the remarkable aspects of this case," Li says. "In fact, he was highly infectious even five months after the initial diagnosis."


This man had a severe autoimmune disease that required him to take drugs to suppress his immune system. So his body couldn't fight off the coronavirus infection as well as a healthy person could. He would get better for a while, and then the virus would counterattack. He would fall sick again. Eventually, he ended up in the intensive care unit. He passed away five months after the initial diagnosis.

Throughout the man's infection, Li and his colleagues ran an illuminating experiment. Every few weeks, the team extracted coronavirus from the man's body and sequenced the virus's genome.

Li couldn't believe what they found. "I was shocked," he says. "When I saw the virus sequences, I knew that we were dealing with something completely different and potentially very important."

The sequences showed Li and his team that the virus was changing very quickly inside the man's body. The virus wasn't picking up just one or two mutations at a time. But rather, it acquired a whole cluster of more than 20 mutations. Scientists had never seen SARS-CoV-2, the coronavirus that causes the disease COVID-19, mutate so quickly during the whole pandemic.


Furthermore, laboratory experiments have shown that some of those mutations help the virus bypass detection by antibodies.

"Toward the very end of his life, he was treated with monoclonal antibodies, from Regeneron," Li says. "And shortly thereafter, we saw evidence that suggested the virus was developing resistance or escaping from these antibodies as well."

Li and his colleagues published their findings in The New England Journal of Medicine in early November 2020 with little fanfare. Then about a month later, the pandemic took a surprising turn — and this peculiar case in Boston took on a new importance.


Scientists in the U.K. and South Africa announced they had detected new variants of the coronavirus. These variants were causing huge surges of COVID-19 in these countries.

When researchers looked at the genes of these variants, guess what they found? A cluster of mutations that looked remarkably similar to the mutations found in the virus from the Boston patient. The sets of mutations weren't exactly identical, but they shared important characteristics. They both had about 20 mutations, and they shared several key ones, including a mutation (N501Y) known to help the virus bind more tightly to human cells and another mutation (E484K) known to help the virus evade antibody detection.

Since Li and his colleagues published their findings, several other teams have reported similar cases in which the virus evolved rapidly inside an immunocompromised person with a chronic coronavirus infection.

"So we have a number of examples, around the planet, in which patients' viruses suddenly have a whole mess of new mutations all at once," says virologist Jeremy Luban at the University of Massachusetts Medical School. And other cases have likely gone undetected, he says.

So scientists are starting to think the two phenomena could be related. That perhaps the new variants arose inside people similar to the man in Boston — that is, people who are immunocompromised and have long-term coronavirus infections.

"I think that's the leading theory," Luban says.

In other words, perhaps the coronavirus uses long-term infections as a mutational testing ground. While inside one person, the virus can try out all these different combinations of mutations and figure out, through trial and error, which ones are best at evading the immune system or helping the virus become more infectious.

Most of these viral versions probably don't spread beyond the chronically infected patient. But every once in a while, as the theory goes, a variant gets lucky, infects a large number of people and launches a new whole stage of the pandemic.

And this process is likely happening again right now, worldwide, in other immunocompromised patients. Eventually, these new variants could mutate again and create even more dangerous forms of the coronavirus.

I hadn't seen that.

[Deleted User 863]

PhD: have you seen this?



Back in the spring of last year, a 45-year-old man went to the Brigham and Women's Hospital in Boston because of a coronavirus infection. Doctors treated him with steroids and discharged him five days later.

But the infection never went away — for 154 days. "He was readmitted to the hospital several times over the subsequent five months for recurrence of his COVID-19 infection and severe pneumonia," says infectious disease doctor Jonathan Li at Harvard Medical School, who helped treat the man.

"So this is an extraordinary individual," Li says.

So extraordinary in fact that this man's case is offering scientists surprising clues about where the new coronavirus variants emerged and why they're causing explosive outbreaks on three continents.

To be clear here, the man wasn't what doctors call a "long hauler," or a person who clears a coronavirus infection and then continues to have health problems for months. This man had living, growing virus in his body for five months, Li says. The same infection lasted for five months.

"That is one of the remarkable aspects of this case," Li says. "In fact, he was highly infectious even five months after the initial diagnosis."


This man had a severe autoimmune disease that required him to take drugs to suppress his immune system. So his body couldn't fight off the coronavirus infection as well as a healthy person could. He would get better for a while, and then the virus would counterattack. He would fall sick again. Eventually, he ended up in the intensive care unit. He passed away five months after the initial diagnosis.

Throughout the man's infection, Li and his colleagues ran an illuminating experiment. Every few weeks, the team extracted coronavirus from the man's body and sequenced the virus's genome.

Li couldn't believe what they found. "I was shocked," he says. "When I saw the virus sequences, I knew that we were dealing with something completely different and potentially very important."

The sequences showed Li and his team that the virus was changing very quickly inside the man's body. The virus wasn't picking up just one or two mutations at a time. But rather, it acquired a whole cluster of more than 20 mutations. Scientists had never seen SARS-CoV-2, the coronavirus that causes the disease COVID-19, mutate so quickly during the whole pandemic.


Furthermore, laboratory experiments have shown that some of those mutations help the virus bypass detection by antibodies.

"Toward the very end of his life, he was treated with monoclonal antibodies, from Regeneron," Li says. "And shortly thereafter, we saw evidence that suggested the virus was developing resistance or escaping from these antibodies as well."

Li and his colleagues published their findings in The New England Journal of Medicine in early November 2020 with little fanfare. Then about a month later, the pandemic took a surprising turn — and this peculiar case in Boston took on a new importance.


Scientists in the U.K. and South Africa announced they had detected new variants of the coronavirus. These variants were causing huge surges of COVID-19 in these countries.

When researchers looked at the genes of these variants, guess what they found? A cluster of mutations that looked remarkably similar to the mutations found in the virus from the Boston patient. The sets of mutations weren't exactly identical, but they shared important characteristics. They both had about 20 mutations, and they shared several key ones, including a mutation (N501Y) known to help the virus bind more tightly to human cells and another mutation (E484K) known to help the virus evade antibody detection.

Since Li and his colleagues published their findings, several other teams have reported similar cases in which the virus evolved rapidly inside an immunocompromised person with a chronic coronavirus infection.

"So we have a number of examples, around the planet, in which patients' viruses suddenly have a whole mess of new mutations all at once," says virologist Jeremy Luban at the University of Massachusetts Medical School. And other cases have likely gone undetected, he says.

So scientists are starting to think the two phenomena could be related. That perhaps the new variants arose inside people similar to the man in Boston — that is, people who are immunocompromised and have long-term coronavirus infections.

"I think that's the leading theory," Luban says.

In other words, perhaps the coronavirus uses long-term infections as a mutational testing ground. While inside one person, the virus can try out all these different combinations of mutations and figure out, through trial and error, which ones are best at evading the immune system or helping the virus become more infectious.

Most of these viral versions probably don't spread beyond the chronically infected patient. But every once in a while, as the theory goes, a variant gets lucky, infects a large number of people and launches a new whole stage of the pandemic.

And this process is likely happening again right now, worldwide, in other immunocompromised patients. Eventually, these new variants could mutate again and create even more dangerous forms of the coronavirus.

I hadn't seen that.

I believe there are also a few similar studies from Europe that found similar things...

Essentially it sounds like "sleeper cells" of mutations that exist within the body and wait until they're needed. The dominant mutations can change over time within the same person based on what the virus needs.

Cool shit. Also scary shit.

Figured you'd understand the science behind it a lot more than us regular folks.

[MICHHAWK]

So, my aunt died of Covid this morning.
I was never a fan of hers, she was a super religious freak.

I remember my cousin and I saved up change to buy some of that fake vampire blood for Halloween. She jerked it out of our hands, called us devil worshippers, and set it on fire. My cousin got a serious whipping over it.

So, I just found out she was sick last night when my cousins' wife IMd me and said that she was in "comfort care". Her husband is on a ventilator.

Last year, she was busy telling my dad that he wouldn't need a vaccine if he accepted Jesus into his heart. He started telling me he was considering starting to go to church.

Well, he hasn't gone to church, and I suppose Jeebus was really busy this morning.

this offering says a heck of a lot more about you than it does your aunt. and it ain't good.

[PhDhawk]

PhD: have you seen this?



Back in the spring of last year, a 45-year-old man went to the Brigham and Women's Hospital in Boston because of a coronavirus infection. Doctors treated him with steroids and discharged him five days later.

But the infection never went away — for 154 days. "He was readmitted to the hospital several times over the subsequent five months for recurrence of his COVID-19 infection and severe pneumonia," says infectious disease doctor Jonathan Li at Harvard Medical School, who helped treat the man.

"So this is an extraordinary individual," Li says.

So extraordinary in fact that this man's case is offering scientists surprising clues about where the new coronavirus variants emerged and why they're causing explosive outbreaks on three continents.

To be clear here, the man wasn't what doctors call a "long hauler," or a person who clears a coronavirus infection and then continues to have health problems for months. This man had living, growing virus in his body for five months, Li says. The same infection lasted for five months.

"That is one of the remarkable aspects of this case," Li says. "In fact, he was highly infectious even five months after the initial diagnosis."


This man had a severe autoimmune disease that required him to take drugs to suppress his immune system. So his body couldn't fight off the coronavirus infection as well as a healthy person could. He would get better for a while, and then the virus would counterattack. He would fall sick again. Eventually, he ended up in the intensive care unit. He passed away five months after the initial diagnosis.

Throughout the man's infection, Li and his colleagues ran an illuminating experiment. Every few weeks, the team extracted coronavirus from the man's body and sequenced the virus's genome.

Li couldn't believe what they found. "I was shocked," he says. "When I saw the virus sequences, I knew that we were dealing with something completely different and potentially very important."

The sequences showed Li and his team that the virus was changing very quickly inside the man's body. The virus wasn't picking up just one or two mutations at a time. But rather, it acquired a whole cluster of more than 20 mutations. Scientists had never seen SARS-CoV-2, the coronavirus that causes the disease COVID-19, mutate so quickly during the whole pandemic.


Furthermore, laboratory experiments have shown that some of those mutations help the virus bypass detection by antibodies.

"Toward the very end of his life, he was treated with monoclonal antibodies, from Regeneron," Li says. "And shortly thereafter, we saw evidence that suggested the virus was developing resistance or escaping from these antibodies as well."

Li and his colleagues published their findings in The New England Journal of Medicine in early November 2020 with little fanfare. Then about a month later, the pandemic took a surprising turn — and this peculiar case in Boston took on a new importance.


Scientists in the U.K. and South Africa announced they had detected new variants of the coronavirus. These variants were causing huge surges of COVID-19 in these countries.

When researchers looked at the genes of these variants, guess what they found? A cluster of mutations that looked remarkably similar to the mutations found in the virus from the Boston patient. The sets of mutations weren't exactly identical, but they shared important characteristics. They both had about 20 mutations, and they shared several key ones, including a mutation (N501Y) known to help the virus bind more tightly to human cells and another mutation (E484K) known to help the virus evade antibody detection.

Since Li and his colleagues published their findings, several other teams have reported similar cases in which the virus evolved rapidly inside an immunocompromised person with a chronic coronavirus infection.

"So we have a number of examples, around the planet, in which patients' viruses suddenly have a whole mess of new mutations all at once," says virologist Jeremy Luban at the University of Massachusetts Medical School. And other cases have likely gone undetected, he says.

So scientists are starting to think the two phenomena could be related. That perhaps the new variants arose inside people similar to the man in Boston — that is, people who are immunocompromised and have long-term coronavirus infections.

"I think that's the leading theory," Luban says.

In other words, perhaps the coronavirus uses long-term infections as a mutational testing ground. While inside one person, the virus can try out all these different combinations of mutations and figure out, through trial and error, which ones are best at evading the immune system or helping the virus become more infectious.

Most of these viral versions probably don't spread beyond the chronically infected patient. But every once in a while, as the theory goes, a variant gets lucky, infects a large number of people and launches a new whole stage of the pandemic.

And this process is likely happening again right now, worldwide, in other immunocompromised patients. Eventually, these new variants could mutate again and create even more dangerous forms of the coronavirus.

I hadn't seen that.

I believe there are also a few similar studies from Europe that found similar things...

Essentially it sounds like "sleeper cells" of mutations that exist within the body and wait until they're needed. The dominant mutations can change over time within the same person based on what the virus needs.

Cool shit. Also scary shit.

Figured you'd understand the science behind it a lot more than us regular folks.

What you're describing and the way it's presented in the article sounds like phase variation, which is something common in pathogenic bacteria for genes that are surface exposed (the ones vulnerable to antibodies). Basically by the time the adaptive immune system amplifies antibodies against it, the pathogen changes the order of the gene sequence, which modifies the amino acid sequence of the protein.

But, that is rearranging chunks of DNA, which would be easily detectable by sequencing. This sounds just like more frequent mutations, but yeah, maybe it serves the same purpose.

I'd be interested in knowing the mechanism behind it. For example most RNA viruses mutate faster than DNA viruses because RNA polymerases don't have a "proofreading" function, but Coronaviruses do, maybe this strain loses that feature, or maybe there's something else that makes it more susceptible to gene deletion or insertion.

Or, it's just that these immunocompromised people stay sick for so long and viral replication is so high that these mutations are just inevitable. Perhaps by having a weaker immune system it allows for a progression of changes rather than immediately selecting them out because an early iteration wasn't cleared like it would have been in a healthy indvidual.

I don't know, I'm speculating, but it sounds interesting.

[Deleted User 887]

So, my aunt died of Covid this morning.
I was never a fan of hers, she was a super religious freak.

I remember my cousin and I saved up change to buy some of that fake vampire blood for Halloween. She jerked it out of our hands, called us devil worshippers, and set it on fire. My cousin got a serious whipping over it.

So, I just found out she was sick last night when my cousins' wife IMd me and said that she was in "comfort care". Her husband is on a ventilator.

Last year, she was busy telling my dad that he wouldn't need a vaccine if he accepted Jesus into his heart. He started telling me he was considering starting to go to church.

Well, he hasn't gone to church, and I suppose Jeebus was really busy this morning.

this offering says a heck of a lot more about you than it does your aunt. and it ain't good.

Can/will you please elaborate what it says about Overlander and why you feel "it ain't good"?

Over/Jeeper/Plano - I'm sorry about your aunt, regardless of your feelings about her.

[Deleted User 863]

it sounds interesting.

I thought so too.

[randylahey]

When an individual is exposed to a new pathogen, that doesn't confer immunity to their offspring. If both your parents had chicken pox, that doesn't make you more immune to it. Your adaptive immune system develops independently over time, based on your exposure to different antigens.

Moreover, the role genetics do play in specific immune response that benefitted individuals during this pandemic might not benefit for the next one, and could even be deleterious.

Once again youre inferring stuff i didnt say. Did I say this? That it guarantees anything for the very next generation. No I did not. Evolution doesn't work that quick

[Overlander]

So, my aunt died of Covid this morning.
I was never a fan of hers, she was a super religious freak.

I remember my cousin and I saved up change to buy some of that fake vampire blood for Halloween. She jerked it out of our hands, called us devil worshippers, and set it on fire. My cousin got a serious whipping over it.

So, I just found out she was sick last night when my cousins' wife IMd me and said that she was in "comfort care". Her husband is on a ventilator.

Last year, she was busy telling my dad that he wouldn't need a vaccine if he accepted Jesus into his heart. He started telling me he was considering starting to go to church.

Well, he hasn't gone to church, and I suppose Jeebus was really busy this morning.

this offering says a heck of a lot more about you than it does your aunt. and it ain't good.

Yeah, you know the whole story from just this post. And your insight is invaluable.
Good job!

[Overlander]

So, my aunt died of Covid this morning.
I was never a fan of hers, she was a super religious freak.

I remember my cousin and I saved up change to buy some of that fake vampire blood for Halloween. She jerked it out of our hands, called us devil worshippers, and set it on fire. My cousin got a serious whipping over it.

So, I just found out she was sick last night when my cousins' wife IMd me and said that she was in "comfort care". Her husband is on a ventilator.

Last year, she was busy telling my dad that he wouldn't need a vaccine if he accepted Jesus into his heart. He started telling me he was considering starting to go to church.

Well, he hasn't gone to church, and I suppose Jeebus was really busy this morning.

this offering says a heck of a lot more about you than it does your aunt. and it ain't good.

Can/will you please elaborate what it says about Overlander and why you feel "it ain't good"?

Over/Jeeper/Plano - I'm sorry about your aunt, regardless of your feelings about her.

I am a bit worried about her husband. He seemed like a good guy. Cuckolded, but overall good.

[Deleted User 863]

this offering says a heck of a lot more about you than it does your aunt. and it ain't good.

Can/will you please elaborate what it says about Overlander and why you feel "it ain't good"?

Over/Jeeper/Plano - I'm sorry about your aunt, regardless of your feelings about her.

I am a bit worried about her husband. He seemed like a good guy. Cuckolded, but overall good.

I am hoping you mean that figuratively and not literally.

[randylahey]

You guys mean well but you are over emphasizing the need for medicine for a virus that leaves the population largely unphased. 99 percent survival rate. Have more faith in natural immune systems, natural selection, and evolution. This isn't something that you need to go all in on the wishes of manipulative politicians to solve

[PhDhawk]

You guys mean well but you are over emphasizing the need for medicine for a virus that leaves the population largely unphased. 99 percent survival rate. Have more faith in natural immune systems, natural selection, and evolution. This isn't something that you need to go all in on the wishes of manipulative politicians to solve

This is the mistake. Politicians didn't make the vaccine.

You're use of unphased AGAIN is wrong. almost 40% of people have serious lingering side effects.

Get a vaccine and that number drops significantly. And the vaccines boost your immune system in the same way that infection does, it just does it without the risk. You clearly don't understand how vaccines work, they work by making your immune system stronger (which is what you profess to want) with respect to a specific pathogen. It's not a chemical drug, you're presenting your immune cells with a shape (antigen) that is identical to shapes on the virus and then your body produces antibodies and T-cells with receptors that recognize those shapes specifically. When you become vaccinated it's your immune system, not a medicine, that makes you immune to the virus.

[PhDhawk]

When an individual is exposed to a new pathogen, that doesn't confer immunity to their offspring. If both your parents had chicken pox, that doesn't make you more immune to it. Your adaptive immune system develops independently over time, based on your exposure to different antigens.

Moreover, the role genetics do play in specific immune response that benefitted individuals during this pandemic might not benefit for the next one, and could even be deleterious.

Once again youre inferring stuff i didnt say. Did I say this? That it guarantees anything for the very next generation. No I did not. Evolution doesn't work that quick

How would it benefit our species if the traits aren't heritable? How does it "strengthen our gene pool" if it's not changing allelic frequencies?

[randylahey]

When an individual is exposed to a new pathogen, that doesn't confer immunity to their offspring. If both your parents had chicken pox, that doesn't make you more immune to it. Your adaptive immune system develops independently over time, based on your exposure to different antigens.

Moreover, the role genetics do play in specific immune response that benefitted individuals during this pandemic might not benefit for the next one, and could even be deleterious.

Once again youre inferring stuff i didnt say. Did I say this? That it guarantees anything for the very next generation. No I did not. Evolution doesn't work that quick

Its not a backpedal. I stand by my statement. Its just you continually inferring people mean something more than what they actually say

[PhDhawk]

How would it benefit our species if the traits aren't heritable? How does it "strengthen our gene pool" if it's not changing allelic frequencies?

[randylahey]

And my use of "unphased" was accurate. I said the population has been unphased. That is referring to the number of people on the planet. The global population has actually continued to rise throughout this pandemic. Approaching 8 billion. Covid is not wiping out humanity. Not even close. Barely phasing us. Be realistic

[sdoyel]

Some of you folks need to let the good Lord get a word in... Too many one-sided conversations about your faith and freedoms are going on.

[randylahey]

And yes. Politicians did not make the vaccine. They funded it and insist on it though and are using it greatly to their advantages

[randylahey]

Government wills always claim to have good reasons for why they need to restrict your rights. Otherwise they couldn't convince people to do it. But at what point will everyone realize their reasons aren't actually that good. Dont be so easily manipulated

[pdub]

I'm guessing randy thinks:
A. the olds were gonna die anyways
B. the 'weak' die preventing them from breeding other 'weak' versions of themselves