The link below is to a cohort study in the UK. The reason for the word "wow" is because of the Cohort size - 17 million. This is high quality data. 40% of the English population were tracked in this. There's some interesting results.
Even correcting for SES non-whites are more at risk from covid-19.
Former smokers are at higher risk HR = 1.25 (95% CI = 1.18-1.33), but current smokers at significantly lower risk of dying of covid-19 although since the hazard ratio of dying of covid-19 is 0.88 (95% CI = 0.79-0.99) and the relative risk of dying of lung cancer something of the order of 100 it's difficult to recommend smoking. Asthma is a risk factor which seems to indicate that the cholinergic agonist theory for nicotine having a protective effect is more likely to be valid - typical drugs for asthma are anti-cholinergics. They found that asthmatics who had recently taken oral corticosteroids had a hazard ratio of 1.25 (95% CI = 1.08-1.44) compared with asthmatics who had not recently taken oral corticosteroids HR = 1.11 (95% CI = 1.02-1.20).
There's good news for people with hypertension as it's not a risk factor, the hazard ratio is 0.95 (95% CI = 0.89-1.01).
Deprivation turns out to be a risk factor independently of the various co-morbidities that they examined - see figure 3.
I think the immediate takeaways for the medical profession are, if a smoker presents with severe Covid-19 give them nicotine replacement. If someone who is taking anti-cholinergic drugs for some reason presents with covid-19 consider dose reduction. If someone is showing signs of cytokine storm then, if it's allowed in medical protocols and not contraindicated, maybe try a cholinergic agonist.
https://www.medrxiv.org/content/10.1101/2020.05.06.20092999v1.full.pdf?fbclid=IwAR2vWByOGj4_4aiyAtz8VNs2ca19D5GaImAOISlI4SA5jdBvj7YfjQvwl90
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@deepthought saidwho cares...smokers are rude and socially incorrect..
The link below is to a cohort study in the UK. The reason for the word "wow" is because of the Cohort size - 17 million. This is high quality data. 40% of the English population were tracked in this. There's some interesting results.
Even correcting for SES non-whites are more at risk from covid-19.
Former smokers are at higher risk HR = 1.25 (95% CI = 1.18-1. ...[text shortened]... /2020.05.06.20092999v1.full.pdf?fbclid=IwAR2vWByOGj4_4aiyAtz8VNs2ca19D5GaImAOISlI4SA5jdBvj7YfjQvwl90
@deepthought saidseems like age is still by far the greatest risk factor. The hazard ratio is nearly off the charts for people over 80, consistent with other findings.
The link below is to a cohort study in the UK. The reason for the word "wow" is because of the Cohort size - 17 million. This is high quality data. 40% of the English population were tracked in this. There's some interesting results.
Even correcting for SES non-whites are more at risk from covid-19.
Former smokers are at higher risk HR = 1.25 (95% CI = 1.18-1. ...[text shortened]... /2020.05.06.20092999v1.full.pdf?fbclid=IwAR2vWByOGj4_4aiyAtz8VNs2ca19D5GaImAOISlI4SA5jdBvj7YfjQvwl90
The age thing, I think, will perplex science for quite some time. In other cases, the reduced immune activity in elderly patients can actually be protective against respiratory diseases like this, since the symptoms are not as acute.
@wildgrass saidPossibly this is due to age reducing the activity of the vagus nerve - to say I don't really understand this is something of an understatement, but what I'm wondering about is something along the lines of: the vagus nerve is implicated in modulating inflammatory immune responses, acute respiratory distress syndrome is caused by massive inflammation, so in old people, whose nervous system isn't as sparky as children's, the vagus nerve doesn't moderate the immune response enough and they go into cytokine storm.
seems like age is still by far the greatest risk factor. The hazard ratio is nearly off the charts for people over 80, consistent with other findings.
The age thing, I think, will perplex science for quite some time. In other cases, the reduced immune activity in elderly patients can actually be protective against respiratory diseases like this, since the symptoms are not as acute.
Another paper of some interest, although this time the group size is tiny, only 20 in each group, compares anti-body responses in recovered Covid-19 patients with historical data from patient who had colds before the outbreak - and so cannot have been infected with SARS-CoV-2 because it hadn't emerged by then. It's not tremendously clear to me whether they're saying that having had a recent cold gives some acquired immunity to SARS-CoV-2 or if they're saying that the immune response to SARS-CoV-2 is similar to the cold and so we might expect Covid-19 survivors to be immune and vaccinations to work.
https://www.cell.com/cell/pdf/S0092-8674(20)30610-3.pdf?fbclid=IwAR1VeP4Zq7DIVKwY7XNhVMuIcts7lIsAhcAEAgGdSqBPfAzPpjpNzgVv-i8
@deepthought saidThat study highlights a lot about what we don't know about this virus.
Another paper of some interest, although this time the group size is tiny, only 20 in each group, compares anti-body responses in recovered Covid-19 patients with historical data from patient who had colds before the outbreak - and so cannot have been infected with SARS-CoV-2 because it hadn't emerged by then. It's not tremendously clear to me whether they're saying that ...[text shortened]... l/pdf/S0092-8674(20)30610-3.pdf?fbclid=IwAR1VeP4Zq7DIVKwY7XNhVMuIcts7lIsAhcAEAgGdSqBPfAzPpjpNzgVv-i8
T cell immunity is fascinating but also complex. The response depends on viral proteins getting degraded and 'presented' on the surface of the infected cell. Other surveillance cells screen these presented proteins for new pieces that haven't been seen before. When new bits of protein are detected, an immune response is triggered. Massive amounts of antibodies and new cells are generated to seek and destroy the invader. Viruses of course develop lots of tricks to avoid detection, by hiding, mutating, slowing their own replication, and pretending to be something else. In this case we have hints but no clear understanding of the dance between it and the immune system.
Antibodies in patients (N=20) that have not been exposed to SARS-CoV-2 can react with the virus-specific proteins in CoV-2. In this study, I didn't see any information on whether they'd had a recent cold. This suggests that some non-exposed patients may have circulating antibodies capable of forming an immune response. Whether they do or not, and whether acquired immunity exists in these patients, is still an outstanding question. This data also suggests that antibody tests for CoV-2 immunity may contain a large number of false-positives (and might not even be possible to develop without substantial errors).
One big caveat is that the study was completely in vitro. They synthesized pieces of the CoV-2 proteins and saw whether it reacted to patient plasma that was frozen back in 2015 or 2018, compared to a small cohort of COVID patients in california. There are many examples, though, of antibodies that can react to small pieces of proteins but do not function in context of the full protein (due to the way proteins fold and other things they interact with).
They also identified regions of the viral proteins that might be better antigens for disease specific immune-response that will benefit vaccine development. In future studies, hopefully, 'epitope mapping' will identify which pieces of the virus are being consistently targeted by human immune system responses. This is a very effective way of narrowing down good chunks that make effective vaccines.
Hope this helps.
@wildgrass saidThanks, that's clarified somewhat. Mixed news then. Anti-body tests may well be problematic, although the one from Roche has been praised. But on the bright side, we may be closer to "herd immunity" (I hate that term, can it be replaced with populational immunity please? ) than we thought.
That study highlights a lot about what we don't know about this virus.
T cell immunity is fascinating but also complex. The response depends on viral proteins getting degraded and 'presented' on the surface of the infected cell. Other surveillance cells screen these presented proteins for new pieces that haven't been seen before. When new bits of protein are detected, an ...[text shortened]... a very effective way of narrowing down good chunks that make effective vaccines.
Hope this helps.
@deepthought saidIn reading this again, they used many different virus proteins to look at antibody reactivity, so of course there would be some antibody cross-reactivity. with the right specific antigen, I think you will get good specificity on antibody tests.
Thanks, that's clarified somewhat. Mixed news then. Anti-body tests may well be problematic, although the one from Roche has been praised. But on the bright side, we may be closer to "herd immunity" (I hate that term, can it be replaced with populational immunity please? ) than we thought.
Herd immunity is unclear and studies vary on location. The new MGH study suggests ~10% of people may have antibodies. It's quite disturbing when you read that more than 100 people at the 175-person Biogen conference walked out sick. You don't hear about that happening with the common cold.
@wildgrass saidI did a quick google search but I'm having trouble finding the MGH study you're referring to, can you provide a link? Based on Office of National Statistics reported deaths registered by the 1st of May (where covid-19 is mentioned on the death certificate, rather than the Public Health England figures which are all cause deaths within 28 days of testing positive for covid-19.), infection fatality rates from the Lancet paper I've cited a few times, and population data for 2018 from the Office of National Statistics - I think 5.87% of the population of England and Wales had been infected by around mid-April (allowing an average of a fortnight from infection to death) and 4.98% the week before. So, allowing for 4 weeks of more recent infections that ~10% figure looks quite realistic to me.
In reading this again, they used many different virus proteins to look at antibody reactivity, so of course there would be some antibody cross-reactivity. with the right specific antigen, I think you will get good specificity on antibody tests.
Herd immunity is unclear and studies vary on location. The new MGH study suggests ~10% of people may have antibodies. It's quite ...[text shortened]... -person Biogen conference walked out sick. You don't hear about that happening with the common cold.
@deepthought saidSorry forgot to post the link:
I did a quick google search but I'm having trouble finding the MGH study you're referring to, can you provide a link? Based on Office of National Statistics reported deaths registered by the 1st of May (where covid-19 is mentioned on the death certificate, rather than the Public Health England figures which are all cause deaths within 28 days of testing positive for covi ...[text shortened]... e. So, allowing for 4 weeks of more recent infections that ~10% figure looks quite realistic to me.
https://www.boston.com/news/coronavirus/2020/05/15/boston-coronavirus-antibody-testing-results
@wildgrass saidLol, walked out sick diagnosed by a doctor? Or fears?
In reading this again, they used many different virus proteins to look at antibody reactivity, so of course there would be some antibody cross-reactivity. with the right specific antigen, I think you will get good specificity on antibody tests.
Herd immunity is unclear and studies vary on location. The new MGH study suggests ~10% of people may have antibodies. It's quite ...[text shortened]... -person Biogen conference walked out sick. You don't hear about that happening with the common cold.
@wildgrass saidty
Sorry forgot to post the link:
https://www.boston.com/news/coronavirus/2020/05/15/boston-coronavirus-antibody-testing-results