This episode is still very relevant for what we are seeing from Omicron now! Here is from herd immunity or the lack of ability to obtain it and why sterilizing immunity for this virus really isn't expected or possible from infection or vaccination. Vaccination is critical to prevent serious illness and can in the short term of months significantly reduce the chances of infection. 33:00 to jump to UK herd immunity discussion etc.
I have a better understanding with what I asked below listening to the next section of the discussion. I don't want any of you guys to waste time on me Thanks so much for your work.
I have one massive complaint, my work efficiency has dropped with all this great content many thanks Professor Racaniello and guests (good to see your also on MSM CNN and RT setting the record straight)!!
I'm trying to understand . With influenza the initial exposure, the strain, influences the adaptive immunity in a discriminatory fashion in once sense, that when we encounter a new stain (antigenic drift) not only are we could be lacking adequate immune response to an unfamiliar strain, because our adaptive immunity is sort of "preoccupied" by generating immune response to the original antigen from the first influenza infection that we ever had? If that is true, could that be in part why someone borne before 1957 might not do well with a vaccine designed for more recent stains like H2N3? Also when the adaptive system is making a memory B cell and T cell response novel Corona viruses which don't have major changes in receptor proteins (like influenza by contrast) but rather evolve by "recombination", each decade since SARS-1? Professor Vincent said (in an earlier TWIV) that a vaccine for SARS-COV-2 might be a one time vaccination like measles. But is it likely that people with SARS-2 antibodies and some (whatever protection is offered) immunity will be in trouble when SARS-3 comes down the pike?
Hello... I am Dr from Iraq I treated 28 patients proved affected with covid-19 I put 14 of the patient steroid treatment in the first week and the other 14 patients I put them on steroid in the second week of the disease , I found all the patient had taken steroid treatment became very well in the second week while the second group of the patients had five deaths while the other still were not cured and some of them finished in hospitals, I hope to solve this problem about the steroid treatment in the first or second week.
You made the point about severity of disease which as a layman seems to me to be an important one. To my untrained mind it seems that with coronaviruses, at least, that the immune system produces antibodies and memory somewhat proportionate to the severity of the disease. An April 6 pre print study of neutralising antibodies in a cohort of 175 people found that around 20% of those with a mild infection produced no detectable antibodies. It also seemed that there was a correlation with age. The older the person the greater the level of neutralising antibodies. Could it be that those people with very mild or asymptomatic infections (typically younger people) are fighting off the virus largely with a strong innate response such that no memory or very short lived memory is created (e.g South Korea and China with some uncertainty regarding small proportions that may have been reinfected). It seems likely that they could become reinfected and potentially transmit asymptomatically more than once. Also this makes any natural herd immunity strategy ridiculous since the very people that produce the best immune response are those that are most likely to die in the first place. This would also have implications for seroprevalance studies. If we're only looking for antibodies to determine the percentage of the population infected, could we miss maybe 20% or more of individuals who had been infected and were asymptomatic and not producing detectable levels of antibodies.
When I first got sick, the orange blossoms were just starting to bloom and I thought my runny nose was from my allergy to those blossoms. I had an unusual headache but I dismissed it. Then, I started having other symptoms but that was a bit later. Anyway, you could end up looking like a COVID patient but you could also get COVID and think it was just allergies if you have a medicine that isn't as long-lasting. I usually take mine in order to sleep well and then just deal with allergies during the day.
The acute blowup of a cold is a cytokine storm, just less of a disaster, and that can be when asthma blows up, and I find if I treat my asthma and my nose fast and hard with my anti-leukotriene and steroid sprays the blowup often never happens. That's the COLD doesn't blow up. I've actually ended up in the ER by easing up on my inhaled steroids if I'm fighting a cold.
I went 115 mph in a 1986 Honda Civic hatchback. If someone can't do faster in a modern Audi, I don't know why they wasted their money on such a fancy car. Anyone who has had to go code 3 on any call knows that you can drive safely a lot faster than the posted speed limit, especially if the traffic is very light, although you should consider someone else who thinks the traffic is light enough to blow through intersections, but you can still usually drive faster than the posted limit quite safely. Of course, fire engines are different because they have 500 gallons of water in them, but the worst vehicle I ever drove fast was a box ambulance and it was really only problematic because the center of gravity was higher. When I was 16, I won a street race only because my car had a lower center of gravity so feeling that in my ambulance wasn't too hard to pick up since I saw from the outside how my buddy had her car on two wheels turning a corner that I did on all four tires. Did I ever drive an ambulance even near that fast? Hell no, but I was well prepared to do so if necessary. Instead, I knew all the shortcuts. Anyway, you should be able to safely make 130 mph or so in a good car on a straightaway.
One other thing; an article in common circulation suggests that inhaled steroids used with asthma have antiviral properties, and it's the sort of statement that makes one go huh?
@@ccmkoho ----- I fear the numbers are going to dramatically worsen. I understand the rationale of the govt, but perhaps the power of this contagion has been underestimated. Hoping for a miracle in Sweden.
May be ,,high altitude oedema,, was caused by low alveolar temperature inducing arteriolare spasm and capillary obstruction by reversibile hemagglutination(by some crioglobulin)
If you're worried about doctors with only a half hour to spare, WHY do you waste so much time chatting? I know it's some arrogant academic thing that actually isn't at all nice - but I can't see a doctor, no matter how upper middle class, having the PATIENCE! Even if one automatically doesn't listen to the first 10 minutes of any talk, you always revert to pure chattering, and upper middle class speech mannerisms, and other time wasters. And frankly, even if we DO have the time, nobody who is on to you and your crazy-making nice-nice upper middle class idiosyncracies wants to hear it! Yick!
This episode is still very relevant for what we are seeing from Omicron now! Here is from herd immunity or the lack of ability to obtain it and why sterilizing immunity for this virus really isn't expected or possible from infection or vaccination. Vaccination is critical to prevent serious illness and can in the short term of months significantly reduce the chances of infection. 33:00 to jump to UK herd immunity discussion etc.
thank you for an informative episode. Got a lot out of this.
Oh, and about WHO, now you know why malignant narcissism is so dangerous.
I have a better understanding with what I asked below listening to the next section of the discussion. I don't want any of you guys to waste time on me Thanks so much for your work.
Thanks for cranking these videos out. Very informative.
Thanks Vincent for another podcast, and Cindy too, job well done!
I have one massive complaint, my work efficiency has dropped with all this great content many thanks Professor Racaniello and guests (good to see your also on MSM CNN and RT setting the record straight)!!
I'm trying to understand . With influenza the initial exposure, the strain, influences the adaptive immunity in a discriminatory fashion in once sense, that when we encounter a new stain (antigenic drift) not only are we could be lacking adequate immune response to an unfamiliar strain, because our adaptive immunity is sort of "preoccupied" by generating immune response to the original antigen from the first influenza infection that we ever had? If that is true, could that be in part why someone borne before 1957 might not do well with a vaccine designed for more recent stains like H2N3? Also when the adaptive system is making a memory B cell and T cell response novel Corona viruses which don't have major changes in receptor proteins (like influenza by contrast) but rather evolve by "recombination", each decade since SARS-1? Professor Vincent said (in an earlier TWIV) that a vaccine for SARS-COV-2 might be a one time vaccination like measles. But is it likely that people with SARS-2 antibodies and some (whatever protection is offered) immunity will be in trouble when SARS-3 comes down the pike?
Hello... I am Dr from Iraq I treated 28 patients proved affected with covid-19 I put 14 of the patient steroid treatment in the first week and the other 14 patients I put them on steroid in the second week of the disease , I found all the patient had taken steroid treatment became very well in the second week while the second group of the patients had five deaths while the other still were not cured and some of them finished in hospitals, I hope to solve this problem about the steroid treatment in the first or second week.
You made the point about severity of disease which as a layman seems to me to be an important one. To my untrained mind it seems that with coronaviruses, at least, that the immune system produces antibodies and memory somewhat proportionate to the severity of the disease. An April 6 pre print study of neutralising antibodies in a cohort of 175 people found that around 20% of those with a mild infection produced no detectable antibodies. It also seemed that there was a correlation with age. The older the person the greater the level of neutralising antibodies. Could it be that those people with very mild or asymptomatic infections (typically younger people) are fighting off the virus largely with a strong innate response such that no memory or very short lived memory is created (e.g South Korea and China with some uncertainty regarding small proportions that may have been reinfected). It seems likely that they could become reinfected and potentially transmit asymptomatically more than once. Also this makes any natural herd immunity strategy ridiculous since the very people that produce the best immune response are those that are most likely to die in the first place. This would also have implications for seroprevalance studies. If we're only looking for antibodies to determine the percentage of the population infected, could we miss maybe 20% or more of individuals who had been infected and were asymptomatic and not producing detectable levels of antibodies.
When I first got sick, the orange blossoms were just starting to bloom and I thought my runny nose was from my allergy to those blossoms. I had an unusual headache but I dismissed it. Then, I started having other symptoms but that was a bit later. Anyway, you could end up looking like a COVID patient but you could also get COVID and think it was just allergies if you have a medicine that isn't as long-lasting. I usually take mine in order to sleep well and then just deal with allergies during the day.
nice discussion but i couldnt able to understand part related to steroids and coaulation
The acute blowup of a cold is a cytokine storm, just less of a disaster, and that can be when asthma blows up, and I find if I treat my asthma and my nose fast and hard with my anti-leukotriene and steroid sprays the blowup often never happens. That's the COLD doesn't blow up. I've actually ended up in the ER by easing up on my inhaled steroids if I'm fighting a cold.
I went 115 mph in a 1986 Honda Civic hatchback. If someone can't do faster in a modern Audi, I don't know why they wasted their money on such a fancy car. Anyone who has had to go code 3 on any call knows that you can drive safely a lot faster than the posted speed limit, especially if the traffic is very light, although you should consider someone else who thinks the traffic is light enough to blow through intersections, but you can still usually drive faster than the posted limit quite safely. Of course, fire engines are different because they have 500 gallons of water in them, but the worst vehicle I ever drove fast was a box ambulance and it was really only problematic because the center of gravity was higher. When I was 16, I won a street race only because my car had a lower center of gravity so feeling that in my ambulance wasn't too hard to pick up since I saw from the outside how my buddy had her car on two wheels turning a corner that I did on all four tires. Did I ever drive an ambulance even near that fast? Hell no, but I was well prepared to do so if necessary. Instead, I knew all the shortcuts. Anyway, you should be able to safely make 130 mph or so in a good car on a straightaway.
I’m not sure if you have the answer for this but what is the time line from infection of Covid-19 to the immunological response to igm to igg?
Please sir make one video on cyclosomes or APC of Cell Cycle.....but immediately
Thank you for information and discussion
One other thing; an article in common circulation suggests that inhaled steroids used with asthma have antiviral properties, and it's the sort of statement that makes one go huh?
Don't tell us in which of your episodes Stanley Proman talked about antibody mediated enhancement and covid!
I understand that antibody mediated enhancement was a real problem with antibodies against SARS1.
Very informative. Thank you.
I had no idea how amazing viruses really are. Now I am hooked. I guess I caught a learning about stuff virus.
Listening on the replay.
Professor...do you or your guests have an opinion on the situation in Sweden? Potential massacre?
@@ccmkoho ----- I fear the numbers are going to dramatically worsen. I understand the rationale of the govt, but perhaps the power of this contagion has been underestimated. Hoping for a miracle in Sweden.
The content starts @8:03
May be ,,high altitude oedema,, was caused by low alveolar temperature inducing arteriolare spasm and capillary obstruction by reversibile hemagglutination(by some crioglobulin)
Or by nitrogen capillary microembolism
Its not HAPE FYI, hypoxia issues are not related to HAPE.
May be some IgM induced by SARS COV2 are haemagglutinant cryoglobuline like.
Why do these women pronounce normal sentences, e.g. 13:33 like questions?!
It's confusing.
Sounds less threatening
If you're worried about doctors with only a half hour to spare, WHY do you waste so much time chatting? I know it's some arrogant academic thing that actually isn't at all nice - but I can't see a doctor, no matter how upper middle class, having the PATIENCE! Even if one automatically doesn't listen to the first 10 minutes of any talk, you always revert to pure chattering, and upper middle class speech mannerisms, and other time wasters. And frankly, even if we DO have the time, nobody who is on to you and your crazy-making nice-nice upper middle class idiosyncracies wants to hear it! Yick!