Depends on if immunity is long-lasting, since cold-causing coronaviruses produce immunity with a tendency to fade over 3 years or so, and if vaccines are an option given that 10 years of SARS vaccine development has generally crashed and burned at the animal testing phase. A highly contagious disease with a 10% hospitalization rate and 2% death rate breathing down your neck for multiple flu seasons sounds rather problematic.
I’ve seen speculation that COVID-19 does not confer meaningful immunity, and we’ve already seen a reinfection. If true, this looks less like “we have a new winter disease” and more like “this is the new normal.”
I remain skeptical of these stories. These people are being tested with excruciatingly sensitive molecular tests after leaving severe disease in a way that is not common in other health contexts. We know that people can shed deactivated measles virus that can be detected by PCR for weeks after they recover. If I was going to guess, I would suspect that what you have is people who got a severe infection with a damaged respiratory system are then coming down with secondary complications while still shedding detectable virus, or their immune system falls apart due to severe complications allowing remnant virus to replicate up to detection levels.
It could be an indication that severe disease can produce a long lingering recovery and you’re not always out of the woods when you are getting better. But the notion of people who had managed to clear the thick hot and heavy infection getting reinfected by a few hundred viral particles from outside their body again so quickly just doesn’t sit well with me. If reinfection happened I would expect it to take years...
I just saw a story suggesting that the COVID-19 is showing signs of a mutation that is very HIV like, making it more likely to infect. This is the second time I’ve read something like that. The other claimed that the structure of this virus made it more likely to bind to a human cell than SARS.
Would like your thoughts if you’ve seen these as well.
I wish news media people would stop with the ‘HIV’ nonsense. Sorry but it just gets on my NERVES at this point.
Every statement having anything to do with HIV goes back to a single preprint that came out a few days after the first genomes, from a lab in India that if this manuscript is any indication has a severe quantity over quality program. The SARS-CoV2 genome has a few percent difference to the SARS genome from a decade ago. There are a couple of small insertions in the protein that the virus particle uses to bind to the human ACE2 protein and gain access to cells for replication. These insertions are indeed a big piece of what makes it so infectious, it binds to human cells much stronger than the SARS virus did. This lab, though, just ran a sequence search and freaked out over the fact that there were matches to these small ~5 amino acid sequences in a few HIV genomes (and didn’t talk about the bacterial and plant genomes you can also find matches in).
They neglected to report something called the ‘expectation value’, the number of times you would expect to find those sequences in a sequence database by random chance. It was high. Short sequences are likely to exist somewhere else in the sequence database by random chance when you dig through all the sequence database in the world, theyre particularly likely to be found in viral sequences that are biased in ther composition, and HIV in particular is something like one fifth of viral sequences on record due to all the research that has been done on it both for disease and biotech purposes and it is hypermutable. The numbers pencil out that you would be surprised NOT to find those sequences in some HIV strain in the databases somewhere. And on top of that, the similar HIV sequences they found are in bits of the HIV sequence that have nothing to do with the function of the protein the insertions are in in the SARS-CoV2 virus.
They also didn’t compare the binding protein to the binding protein of any coronaviruses other than the SARS virus from a few years back. There is a wild virus sequenced from a bat that has a common ancestor with this virus about fifty years ago and has these insertions, plus or minus a few mutations.
And of course, nobody noticed that another similarly low-quality preprint noticed that a piece of one of the proteins vaguely resembled a 20 base pair piece of intergenic DNA from a fish. With a similarly high expectation value. And all the same problems but didn’t get the dogpile because it didn’t make people freak out.
So yes, there are insertions in the protein that are part of how this virus manages to bind incredibly strongly to the human ACE2 protein and be extremely infectious and contagious. They have NOTHING TO DO WITH HIV and I wish the news would stop parroting that preprint, which within 48 hours was dogpiled by scientists telling the authors that the conclusions about everything but the sequence itself was bullshit to the point that they published the preprint equivalent of an erratum.
I can get why this gets on your nerves (very complex subject that few understand—I don’t).
Thanks for share and sorry to be part of the problem. The key for me was the increase ability to bind with human cells which seems to be true. The “fake news” connection with HIV cannot help and clearly was not needed.
Thanks for the more technical details! Really glad we have someone like you participating here.
Depends on if immunity is long-lasting, since cold-causing coronaviruses produce immunity with a tendency to fade over 3 years or so, and if vaccines are an option given that 10 years of SARS vaccine development has generally crashed and burned at the animal testing phase. A highly contagious disease with a 10% hospitalization rate and 2% death rate breathing down your neck for multiple flu seasons sounds rather problematic.
I’ve seen speculation that COVID-19 does not confer meaningful immunity, and we’ve already seen a reinfection. If true, this looks less like “we have a new winter disease” and more like “this is the new normal.”
I remain skeptical of these stories. These people are being tested with excruciatingly sensitive molecular tests after leaving severe disease in a way that is not common in other health contexts. We know that people can shed deactivated measles virus that can be detected by PCR for weeks after they recover. If I was going to guess, I would suspect that what you have is people who got a severe infection with a damaged respiratory system are then coming down with secondary complications while still shedding detectable virus, or their immune system falls apart due to severe complications allowing remnant virus to replicate up to detection levels.
It could be an indication that severe disease can produce a long lingering recovery and you’re not always out of the woods when you are getting better. But the notion of people who had managed to clear the thick hot and heavy infection getting reinfected by a few hundred viral particles from outside their body again so quickly just doesn’t sit well with me. If reinfection happened I would expect it to take years...
I just saw a story suggesting that the COVID-19 is showing signs of a mutation that is very HIV like, making it more likely to infect. This is the second time I’ve read something like that. The other claimed that the structure of this virus made it more likely to bind to a human cell than SARS.
Would like your thoughts if you’ve seen these as well.
I wish news media people would stop with the ‘HIV’ nonsense. Sorry but it just gets on my NERVES at this point.
Every statement having anything to do with HIV goes back to a single preprint that came out a few days after the first genomes, from a lab in India that if this manuscript is any indication has a severe quantity over quality program. The SARS-CoV2 genome has a few percent difference to the SARS genome from a decade ago. There are a couple of small insertions in the protein that the virus particle uses to bind to the human ACE2 protein and gain access to cells for replication. These insertions are indeed a big piece of what makes it so infectious, it binds to human cells much stronger than the SARS virus did. This lab, though, just ran a sequence search and freaked out over the fact that there were matches to these small ~5 amino acid sequences in a few HIV genomes (and didn’t talk about the bacterial and plant genomes you can also find matches in).
They neglected to report something called the ‘expectation value’, the number of times you would expect to find those sequences in a sequence database by random chance. It was high. Short sequences are likely to exist somewhere else in the sequence database by random chance when you dig through all the sequence database in the world, theyre particularly likely to be found in viral sequences that are biased in ther composition, and HIV in particular is something like one fifth of viral sequences on record due to all the research that has been done on it both for disease and biotech purposes and it is hypermutable. The numbers pencil out that you would be surprised NOT to find those sequences in some HIV strain in the databases somewhere. And on top of that, the similar HIV sequences they found are in bits of the HIV sequence that have nothing to do with the function of the protein the insertions are in in the SARS-CoV2 virus.
They also didn’t compare the binding protein to the binding protein of any coronaviruses other than the SARS virus from a few years back. There is a wild virus sequenced from a bat that has a common ancestor with this virus about fifty years ago and has these insertions, plus or minus a few mutations.
And of course, nobody noticed that another similarly low-quality preprint noticed that a piece of one of the proteins vaguely resembled a 20 base pair piece of intergenic DNA from a fish. With a similarly high expectation value. And all the same problems but didn’t get the dogpile because it didn’t make people freak out.
So yes, there are insertions in the protein that are part of how this virus manages to bind incredibly strongly to the human ACE2 protein and be extremely infectious and contagious. They have NOTHING TO DO WITH HIV and I wish the news would stop parroting that preprint, which within 48 hours was dogpiled by scientists telling the authors that the conclusions about everything but the sequence itself was bullshit to the point that they published the preprint equivalent of an erratum.
I can get why this gets on your nerves (very complex subject that few understand—I don’t).
Thanks for share and sorry to be part of the problem. The key for me was the increase ability to bind with human cells which seems to be true. The “fake news” connection with HIV cannot help and clearly was not needed.
Thanks for the more technical details! Really glad we have someone like you participating here.