Read a report saying people with O type blood, positive or negative, are less prone to catching the virus and/or have less symptoms if they do. Also, as a percentage, more Hispanics than all other groups have O blood, and more blacks percentage wise have O blood than whites.
First, is this accurate? If so and all other things being equal, will we see more Caucasians catch the virus versus other groups?
The blood type thing MAY end up being a player, but perhaps not. As an A+ (think I read A makes SARS-CoV2-2019 very happy, supposedly), I ponder it... But not as much as I do trying to generally take good care of myself and be safe when out and about.
I'd need to see a lot more on this to discover if it's a real finding, or coincidental.
Unfortunately, far too many of the reports touted by the media are problematic. First, most of the reports are preliminary and have not gone through any peer review. Even worse, the people reporting on these pre-pub reports have absolutely no science background. Journalists are not required to take courses in math or any of the hard sciences to become "reporters".
The effect of blood groups is just one factor. Other factors go into the mix as to whether one will get Covid...age, obesity, blood pressure, diabetes, COPD and other lung conditions, asthma, etc. If all other factors were equal, there is probably a slight advantage for having group O...emphasis on slight.
Had discussion with my physician this week and (especially for my age) the biggest factor is overall physical health and actual exposure. Common sense and good hygiene are far the best preventative.
Unless you actually have covid, masks are a psychological tool. After blogjoggin and reading media reports where masks are being made mandatory, not one single article or governmental dictate made any mention of the proper use of masks. For example, paper masks loose effectiveness once the moisture in ones breath make them moist and need to be replaced periodically (less than an hour). Studies have shown that people tend to touch their faces more often when wearing one. And they should be removed from the inside after one washes their hands. Handmade cloth ones are the biggest danger as they filter nothing and one will re-breath any particles that are exhaled.
My wife and I were career life scientists (I a immunogeneticist and my wife a veterinary virologist) and spent much time being trained and using personal protective equipment in the lab. We see the majority of those wearing masks in public using them improperly and making their efforts worthless. There are probably as many dangers wearing masks as perceived protections.
Politicians and media assure us that contact at protests and demonstrations give no risk, but church and Trump rallies will doom you. (!!!)
You need to just go away and take your anger somewhere else.
Jack, thanks. The blood report keeps hitting certain circles. And I mentioned all other things for a reason.
From a lay person's perspective, there are lots of studies going on and even scientists look like they are discovering new information.
That is an interesting thought. How does the virus know what conditions a host has upon contact? If a host did not have any of those factors, couldn't they still get sick? I didn't think the virus discriminated...or was only attracted to certain conditions??
K Cummings's Link
However, how a person with those other conditions reacts to the infection (eg: cytokine storm), and their ability to fight it off is different.
At least that's what I've read.
Mike in CT's Link
Good questions and apologies for my tardy reply; yesterday I was pretty much fried by dinnertime as I spent a good chunk of the day working with the flagship hospital in the largest VISN (Veterans Integrated Service Network for those not in the military, or VA hospital system) as they are struggling on how to best mitigate the effects of COVID-19.
Will, Jack and Kevin have all touched on key points and I'll try to add a bit more.
First, as Jack mentioned blood type may have a slight impact but absent a well-constructed, peer-reviewed study at best the information is purely anecdotal and at worst it could turn out to be misleading. A great example would be the efficacy of hydroxychloroquine (HCQ) as a treatment option for COVID-19. Initially we were shown articles that appeared to indicate great potential only to find those were poorly constructed and not peer-reviewed. A month or so ago we saw articles saying the opposite was true and some saying the side effects were far too severe to ever warrant its use. Very recently we swung back towards it being effective with some studies having been well constructed and pending peer review.
The big question is how do people get infected and why are there differences in the severity of the infection. Aside from the factors already mentioned there are 2 very important ones; viral load when exposed and the number and affinity of host receptor cells for the virus.
Viral load (the number of virus in an infected person) directly relates to that persons ability to infect others; asymptomatic people for example may have very small viral loads and their ability to infect others is lower than those with moderate to high viral loads. As a persons viral load increases the infectious material they expel (droplet nuclei for example) contain more virus, hence they have a higher probability of infecting those exposed to them.
The second factor is the number and affinity of host receptor cells for the virus; THE critical stage in any viral disease centers on the viruses ability to enter a host receptor cell and begin the process of replicating itself. It was noted early on that the pediatric population, and especially the very young seemed far less likely to become infected; researchers quickly determined this was due to their having fewer receptor cells than adults and also those cells not being fully-developed relative to what they would be in adulthood.
When I speak of affinity of a host receptor cell for a virus think of it this way; if you had a jigsaw puzzle there are obviously pieces that fit perfectly, pieces that are very close but not quite right and you progress to pieces that don't come close to fitting. Receptor cells can mimic this characteristic too; the better the fit the higher the likelihood the virus achieves its primary objective of entering a host receptor cell and corrupting that cells means of replicating its own genetic material (DNA or RNA) and getting that cell to replicate the viruses genetic material instead, turning that host receptor cell into a virus-making factory if you will. The higher the affinity the more cells are infected, the more virus copies are produced, the higher viral load, etc.
Now as to the severity of the infection again, the key factors have been touched on so I won't rehash them, just re-emphasize that these are key determinants as to the severity of the infection a person gets.
I'm going to insert a link in the post to a promising study about using the viruses need to replicate against it; it's a very ingenious approach and it has shown great potential in vitro (in a petri dish to be precise). In theory this should work in vivo (in the body) and if it can be done it would be a great asset in the fight against this disease. I see a lot of studies of this nature and while the enthusiasm for presenting this type of information is understandable great care needs to be taken in HOW this kind of information is shared; if it isn't put in proper context (e.g. "not peer-reviewed", "in vitro data only", "not a randomized controlled study" it can be misleading or even dangerous (misuse of a treatment can be as bad as any disease, or unknown side-effects will manifest only when given to people).
I'm going to circle back to your question about blood types as I just mentioned a critical component of any study; being a randomized controlled study. In your question you asked about the impact of a particular blood type. If you are looking for one particular factor and it's impact on the ability of a virus to infect or it's relation to disease severity then you need to construct your study to be of 2 groups; a control group (where you don't incorporate this one factor or don't eliminate any other co-existing factors) and a trial group (all other factors are accounted for).
By accounting for all other factors in the trial group a researcher can compare the outcomes in that group to the outcomes in the control group; positive outcomes can then be ascribed to the one isolated factor, in your question, a specific blood type. It should be noted that you can also account for negative effects by this means too; for example, side-effects of a drug; the control group gets a placebo instead of the drug so any negative effects can be attributed to the drug (as could positive benefits, such as the studies showing promise for HCQ).
I hope this is helpful and as always, please feel free to ask any questions or bring up for discussion any new information you come across.
Yes, your explanations always make sense to us with limited knowledge. What really caused me to ask this is I am O+. I am a regular blood donor but have been recently hit with multiple emails, texts and phone calls from our Community Blood Center that they have an urgent need for me to donate, a significantly higher volume of contacts than normal. I thought it might have something to do with this but did not understand why. My interest is still piqued as Robin needs to schedule two knee replacements over the next year but the surgeon and hospital are remaining non-committal as to dates, informing her because of Covid it is tough to schedule now. Just thought it was odd with less medical procedures being undertaken that there is a more urgent need for blood.
Thank you again.
I suspect there are a couple of reasons why you've been bombarded with requests to donate blood; O-positive is the most prevalent blood type so there would be the greatest need for this type; the pandemic has impacted donations and as the blood supply is used throughout all 50 states it's possible areas that are relatively stable may look to residents to "pick up the slack" for areas where due to prevalence people aren't lining up to donate as they used to do.
Another reason could relate to some of the complications of COVID-19 infection, anemia being one and one that would require blood products (transfusion, FFP (Fresh frozen plasma), etc.) to help stabilize patients.
If you were O-negative (universal donor) I suspect you might have your own personal escort ready to drive you to the blood donor center 24/7....
Thanks and you are most welcome!
Hope you and yours are and remain well!
Habitat for Wildlife's Link
Covid should not be, but is a political issue. Wearing or not, facemasks have become contentious.
Lots of other variables at play, and consider the source here, but Slovakia and other eastern-European countries have had lower infection rates. Notably there appears to be a correlation between wearing and lower rates.
Asking you to forget the politics, and asking now because Trump wore one yesterday. They are not fool proof, but should we all be wearing one in public? Thanks.
I couldn't agree more.
In addition, it is always a crap shoot when you attempt to compare what we are seeing here in the US to other countries.
In my opinion, unless all parameters are the same, it simply doesn't mean anything.
It's a lot like all the bow speed comparisons you see over on the LW. If one is done with 6 gpp of arrow weight and a 30" draw and one is done with 12 gpp of arrow weight and 27" draw, they don't mean squat.
How much testing is being done, who is being tested (anyone vs only symptomatic people), accuracy of the test itself, what is considered a "covid death," demographics, population density, etc., etc., etc..
Slovakia was mentioned earlier with a total population of about 5.5 million people. It's largest city has a population density of 3,000 per square mile vs NY at 27,000 per square mile.
How many people are they actually testing and why?
At the end of the day, if you want to make a case for the current administration doing everything right, you could. If you wanted to make a case for the current administration doing everything wrong, you could.
When Mike in CT says that all things considered we've done a pretty darn good job, I believe him.
People versed in working with numbers can hold many of the variables constant, or adjust for the differences (such as population densities) across different samples. This allows an educated guess on the variances between samples, and what may be the cause. I have read after adjusting and comparing Slovakia with other countries of varying densities and other variables, their rates of infection are below expected rates, based on averages observed across all samples. This technique, admittedly with limited data and always suspect and not peer reviewed as of yet that I am aware of, MIGHT suggest the early implementation of masks, social distancing, improved hygiene etc. had a positive impact on containment.
I don't want this to be political. Mr. Trump wore a mask yesterday and there was one report that he has concerns that people who think this is all a hoax might not get vaccinated when it becomes a reality. Hopeful that maybe spreading (odd choice of word eh?) sound knowledge will help overcome this barrier, of which I am in agreement with our president on.
K Cummings's Link
When (if) you have time, would you care to opine on the piece at the attached link.
I know nothing about the source but thought it might be interesting to hear your take on his opinion.
This is a very sound explanation of what went wrong at the outset of this pandemic and how a lack of understanding about the principles of a test have continued a well-intentioned but misguided management policy.
The author is absolutely correct in asserting that there is plenty of evidence to suggest there was some level of immunity already present; this makes perfect sense as being a member of Coronaviridae (Coronaviruses) there will be certain antigenic similarities between members of that family. The closer the "relation" of SARS-CoV-2 to these other family members the greater the level of protection in the community.
Two points in the article are especially significant; the ordering and subsequent reporting of tests without fully understanding the nature of those tests and what a positive result actually means (I mentioned this critical point to a poster in another thread as some of you may recall).
Molecular assays have been both a boon and a curse in medical diagnostics; a boon as they are incredibly sensitive and can detect very low amounts of the target; a curse because of that very reason; they detect a target, not necessarily viable (living) target.
In the case of SARS-CoV-2 the target(s) is (are) viral proteins, most commonly the "spikes" by which they attach to host receptor cells. Obviously these spikes are present in complete, viable virus but they can remain after a component of our immune response has destroyed the viable virus leaving remnants of it behind.
In my earlier response I alluded to a misconception in the lay community about "false positive" tests; in the sense of disease not being present positive results do constitute a false positive but in terms of detecting the target protein(s) they are truly positive; they have done exactly what they were designed to do. The test simply does not "know" if the virus is intact and viable or merely remaining fragments of a dead virus that is completely incapable of producing infection.
This is why the first critical interpretative point in the spike in cases is to understand the test methodology employed. I have no doubt that this is at least partially why we are seeing a significant spike in the number of cases diagnosed but a decline in the initial mortality rate (and as I've mentioned earlier some of this decrease in mortality may also be due to the virus mutating to a less virulent form.)
The last critical point referenced the impact of an aspect of our immune response (after antibodies have been depleted, or if they are lacking) specialized white blood cells (T-cells) seek out and destroy host cells containing the virus. When this immune response ramps up significantly we get what the author refers to as a "cytokine storm" and this can lead to organ failure and via that path, death.
In short, what we saw in the initial wave were a lot of deaths due to this cytokine storm and another reason we've seen a reduction is the recognition of this reality led doctors to adapt their treatment to manage this aspect; one approach involved using immunosuppressive approaches to mitigate the cytokine storm (a decrease in ventilation has also occurred as it was realized a high number of patients never came off of the ventilator (this occurs with a variety of other conditions seen in an ICU as well by the way) as intubation predisposes patients to a number of nosocomial (hospital-acquired) infections.
That last sentence may provoke a "light bulb" moment in all of you who have questioned if deaths attributed to COVID-19 might have been caused by something else. Take a bow; ventilator-associated pneumonia can occur in intubated patients owing to a robust population of some nasty bacteria that exist in hospitals, some of which are also very resistant to antibiotics. This scenario harkens to the phrase "the cure is worse than the disease."
I would highly recommend not only reading this paper but sharing it; this is a great source of what an objective medical/scientific examination of a disease should look like.
Thanks for sharing Kevin!
There are a number of good reasons for wearing a mask properly (e.g. correct type, proper fit, etc.) and there are definite preventative values to the practice.
I wear one when I got to the grocery store, Home Depot or when I call on a hospital (and many now have this as a requirement along with a host of screening protocols).
An ounce of prevention....
The article sounded plausible but I wanted to make sure. Pretty fascinating stuff for sure.
""Doris Loh Jul 10
Indeed, "EVERYONE" was wrong, including the author of this article.
This disease is not your common flu virus because it is no longer a respiratory disease but a blood vessel disease.
This disease did not produce the massive number of deaths predicted. Instead this disease is shocking everyone with unexpected blood clots found in every blood vessel and organ upon autopsy.
This disease has very little to do with ACE2 receptors, as everyone claimed. Instead, more studies are now saying they can't find ACE2 mRNA expression in relevant sites of major organs and tissues where the virus attacks, including lungs, blood vessels and platelets. You can't have a blood clot without platelets, you know. And if ACE2 is not expressed in platelets, how does the virus cause platelet dysfunctions? Nobody's got that one figured out yet.
This disease is taking longer to recover from. Read the long-haul stories, three months and counting....fatigue, memory loss, vision loss, pain, anosmia....
This disease is producing all kinds of unexpected damages in the brain that no one anticipated. These damages cause demyelination similar to multiple sclerosis. Did anyone say COVID-19 can be like MS? Wait a few months and find out.
This disease is not producing antibodies as expected (only 4 to 5% in the infected according to several major studies involving large cohorts). Why?
Because this coronavirus uses a receptor that is part of the super immunoglobulin family, CD147.
Yes, EVERYONE got it wrong.""
I read the comments from Doris Loh and while she correctly identifies certain manifestations she is incorrect when she assigns a cause to those or disputes claims about the mechanism of the disease. I'm providing links to 3 different articles that address some of these points and will speak briefly to some of her objections.
1. The disease is not your common cold or flu; the author did not state this but instead correctly pointed out that the SARS-CoV-2 virus is a member of the family Coronaviridae from which about 20% of our common colds are derived. The author is correct to assert there could be at least minimal level of antibody protection owing to the potential for antigenic similarity.
2. Blood clots; one of the links addresses this but Doris completely missed the point of this being a direct complication of COVID-19, specifically the cytokine storm I referenced.
3. CD-147 vs ACE-2 receptors; early articles (some earlier still than the one I'm providing) reference both receptors and affinity for SARS-CoV-2 has been demonstrated in both; citing non-peer reviewed and non-randomized controlled studies is one of the vehicles that generated so much confusion and still does today.
4. Her points about time to recovery and other "unforeseen" side-effects point out her completely missing the ramifications of a cytokine storm.
5. I have no idea what sources she cited (or read) to arrive at her claims about antibody production but not only are there studies showing the opposite but there is a treatment modality that uses convalescent sera (from patients who had COVID-19 and recovered and have antibodies). The article I'm providing the link to is just under 2 weeks old.
6. CD-147 is associated with T-cells, the cells responsible for the cytokine storm that was a leading contributor to COVID-19 fatalities.
In the scientific community there are no shortage of egos; I have come across too many instances of articles or publications being attacked not on the basis of the soundness or lack thereof of the science but because someone's sacred cow was being gored. Based on some of the reasoning errors and positions contradicted by the evidence I wonder if that is the case here.
Apologies for an important omission regarding host cell receptors; Doris claims it is CD-147, not ACE-2 receptors involved in COVID-19 infections.
Here is the gigantic problem with that thesis; at birth, barring of course any genetic issues by the age of 2-3 months an infant has a well-developed immune system (the time in between birth and then is when a mother's passed on antibodies via breast milk aid the newborn). If Doris's thesis were correct that CD-147 is the only (or even the primary) host receptor for SARS-CoV-2 then infants would rank at or near the top in terms of % of infections; obviously we know they don't so that begs the question why?
ACE-2 receptors are both less developed and in far fewer numbers than adults; if ACE-2 receptors are not involved in COVID-19 infection than this point would be irrelevant to the rate of infection in the very young; the fact that the very young who have a fully functioning immune system at 2-3 months but have fewer ACE-2 (and less developed than adults) receptor cells points clearly to those receptors role in acquiring the infection.
Her thesis fails on a basic physiological level; the evidence supports the opposite of what she claims.
Just by coincidence I was going thru my online lab results for an ongoing VA disability claim I'm working on. Some of the explanations for some of the blood lab results are related to what we're talking about here. I snipped it as others following this thread might find it useful.
Pig Doc's Link
That will be wonderful if it is true, and I hope it is!
Absolutely. Real data, science, and math doesn't lie. Politicians and bureaucrats do...
I was thinking about something this morning and would like your opinion if you don't mind.
Have you ever noticed how many meteorologists react to the possibility of a hurricane, a tornado, or even just a severe storm? How often is the actual event worse, or even close to what has been reported?
It almost seems that because of the relatively infrequency of these events, just the prospect of one of them occurring turns into their "super bowl" (for lack of a better term) and therefore they trip over themselves trying to outdo each other warning of the possible impending disaster.
In your opinion, does the same phenomena occur within your field? In other words, does the "super bowl" effect apply to the extent that epidemiologists and other health care professionals do the same?
I know it happens in my field. During every market correction, the "experts" literally can't wait to get to a microphone to warn everyone about the impending economic disaster and the next great depression.
Let's face it, it's not like pandemics happen every day. Is it "game time" for some when it comes to predicting the impending disaster?
It has just come to light that, in Florida, several labs reported almost 100% positive test results. When questioned about those results, they revised their positive results to less than 10%.
Why is this information not front and center on all news media sources?
I agree on the media, that's a given. There's a reason they say "if it bleeds it leads." Heck, if it doesn't bleed, they'll make it bleed.
I'm more interested in what Mike's opinion was regarding the actions of the trained professionals in the field.
On the whole I don't think those in my field tend to overreact to events such as this; I say on the whole, as in keeping with the meteorological theme this particular event became "the perfect storm" for a media that has been a de facto arm of the Democrat party for years and might better labeled as "The Ministry of Propaganda" as that is a more accurate description of today's MSM.
It is the media that has the most skin in this game as they rival, if not exceed the pathological hatred many Democrats feel about Donald Trump. To them, this presented perhaps their last, best chance to defeat him this November. Look at the political reality at the onset of 2020; this was as close to a mortal lock as could be and every politician and every pundit who covers politics knew it.
Russiagate had failed, impeachment had failed, obstruction at every turn had failed; what card remained to be played? Nature provided what I'm sure many who despise Trump viewed as the ultimate "trump" card (pardon the pun); given the proper framing of the narrative this could be Trump's Waterloo and that has been the theme of the MSM narrative from Day 1, 24/7.
The greatest danger we face is not lies but half-truths; lies are easily discerned but half-truths, owing to that portion that is true can work remarkably well owing to the overall intellectual laziness of the American public; too many people simply can't be bothered to check the veracity of what the media reports. The MSM knows this and they count on it; a quick anecdotal scanning of most of our memories over the past 3 years should lead us to conclude we've seen a lot of "news stories" shredded with a simple fact check; surely most must realize this is not coincidence; this is blind, pathological hatred of one man-Donald Trump.
When we only hear about the number of new cases but no mention is made of how many of those are simply an overly sensitive test detecting viral fragments and these "new cases" don't represent actual infection or even the threat of infectious spread that is a disinformation campaign that would make Joseph Goebbels look like a rank amateur.
While disappointed in what's going on I am not disheartened; this all-in, all-or-nothing strategy is going to implode, simply on the basis of the fact that this virus hasn't gotten the memo; it will run its course as all viruses do and the "sky-is-falling" meme will collapse under the sheer weight of its absurdity.
Stay well and keep the faith-this too shall pass....
As to the rest of what you said, I couldn't agree more. I honestly believe that no matter the outcome, Nov. 4 will bring an entirely new narrative when it comes to covid19.
I just pray that enough people see the propaganda for what it is so as to make an informed decision.
Is there any truth to the fact that what is not being reported is folks who survived but are facing "rehabilitation" issues. Mike, I reported to you the patient of Robin's who 3 months after infection still has lung capacity issues that his doctor said will be present for the rest of his life.
I have a friend with a relative who has balance issues making walking difficult, supposedly from the covid impact on his brain. He said there were several at the rehab center with varying "covid conditions"
Is there any truth to this being a larger concern that is just not getting attention as of yet?
It's not everyone, but there does seem to be a long drag back for some - or longer term issues... But it's a disease that's really been studied for only about 7 months at this point... So pretty hard for folks to firmly be able to say much RE the longer term.
As far as risk factors go, it goes from 1) age to 2) BMI >39 last I saw a few weeks ago.
Such an excellent point about the shortness of time this specific virus has been studied. That to me is part of the challenge right now because as we learn more our knowledge "adjusts" and causes confusion, especially with folks who are only tuned in now and again.
We hear talk, valid, about the economic costs of shutting down. But if this virus negatively impacts the long term health of a sizable portion of our work force thereby reducing productivity, that will also have to be considered as a long term economic cost.
To Will's point we haven't had the kind of time necessary to have a true handle on the long-term impact of having had COVID-19 infection. As we sit here today there are some things we do know; there are patients who develop AKI (acute kidney injury; once referred to as Acute renal failure) and for some this may consign them to a lifetime of dialysis, a costly treatment and one that obviously places limitations on that persons life.
The cytokine storm that may arise as a result of infection can also lead to long-term damage to the lungs leaving patients with decreased pulmonary function and there are other organs such as the liver that can be impacted; as the liver is key to so many bodily functions any compromise to it's functionality will have long-term effects on the quality of life for those patients.
Some of the issues I just mentioned we may be able to mitigate if not prevent as we gain in understanding, not just of the disease but how different approaches to treatment may lead to more favorable or at least, less adverse long-term outcomes.
We are all going to be impacted by this virus for at least the next couple of years; a colleague of mine shared a conversation he had with a Chief of Cardiothoracic Surgery at a large teaching hospital about when things might "get back to normal." The surgeon told him he didn't think this would happen until next summer, reason being he doesn't see us having a fully-vetted vaccine before Q1 2021 and it will take time to vaccinate a sizable percentage of the population and he felt herd immunity would take care of the rest.
Bottom line, in his opinion it's going to be somewhere between 11-13 months before we can all exhale.
Thanks, and that's what some sources of mine are saying. However, might be a promising vaccine development happening in the UK.
It has a direct correlation to longevity and seems to have a direct correlation to COVID death. It's true that some people with high BMI are healthier than some people with the same BMI because they are more fit and have muscle in place of fat. But the fact remains, big muscular people die younger, usually of cardiovascular disease, than skinny people.
It works for most people because big people, whether they be fat or muscular, seem to not live as long. Centenarians are most commonly short, skinny people. And not just at 100 because they lost height.
It (BMI studies) doesn't work as well for people who lift weights to gain muscle, but those people rarely are as big as they age as they are during youth to middle age and they're a minority of the population as the average person who has a BMI >34, even >29 in America, has a body fat percentage that is not healthy or at least not ideal as far as longevity is concerned.
EDIT: On another front, Mike makes a really good point that is so difficult to properly underscore or quantify, in that we're on the bleeding edge of knowledge here. It's so early. We know more every day. I suspect, a couple years from now, we'll know so much more that we'll look back at 7/20/2020 and shake our heads. Hide sight is 20/20, but we just need so much more time for the research to happen - and it's happening at an incredible rate.
It's okay to mask shame but fat shaming is unacceptable, Ike!
K Cummings's Link
I posted this video on the "Flatten The Curve" thread but I thought I would post it here too.
It's somewhat long, but if you have the time, your opinion would be appreciated.