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Maciamo
04-08-09, 10:43
Blood types do not exist just to create conversation between people ("What's your blood type ? Really ? Me too !") or for the Japanese to try to predict your personality (http://en.wikipedia.org/wiki/Blood_types_in_Japanese_culture). They actually have a vital immunological function. They help us fight diseases.

Their distribution can tell us what major disease epidemics a given population suffered in its recent history (e.g. in the last thousand years). For example, most native Americans belong to group O. It is believed that this is due to a syphilis epidemics and that the O type were better are fighting off the disease.

There is no ideal blood type though. Each type has its pros and cons.

Group A and B make people more resistant to cholera, while AB confers the most resistance. O offers virtually no immunity against cholera.

B confers weaker protection against plague. This is probably why B is more common in North-East Europe, which was virtually unaffected by the Black Death (http://en.wikipedia.org/wiki/File:Bubonic_plague-en.svg) during the Middle Ages.

A-type carriers are the most likely to survive plague, but suffer from a higher rate of heart disease, because their blood is more likely to clot. They are also at increased risk of contracting smallpox and developing cancer of the esophagus, pancreas, and stomach.

Type O, contrarily to A, is slightly protective against cardiovascular problems. It also boosts resistance against tuberculosis (TB), but increases the risk of venous thromboembolism and developing duodenal and peptic ulcers. It also attracts more mosquitoes (through which malaria is transmitted).

A recent study (http://spittoon.23andme.com/2009/08/03/snpwatch-genomewide-study-supports-blood-type-as-a-risk-factor-for-pancreatic-cancer/) revealed that people with type O blood are less likely to get pancreatic cancer, but also (http://spittoon.23andme.com/2009/08/06/abo-blood-type-important-for-more-than-just-transfusions/) stomach, breast, ovarian and cervical cancer.

Humans are not the only ones to have an ABO system. Apes have the same antigens on their red blood cells. Gorillas are almost always B, exceptionally O, but never A or AB. Chimpanzees most usually belong to A, occasionally to O, but never to B or AB. Orang-utans seem to lack the O type altogether.

Other antigen systems

The ABO blood group system isn't the only antigen system found in humans. There are about 30 human blood type systems (http://en.wikipedia.org/wiki/Human_blood_group_systems): Rhesus, Kell, Diego, Duffy, Kidd, and so on. Each have a role in immunity. Some are found only in some specific populations and completely absent elsewhere. This is the case of Diego antigens, found only (at low frequency) among Mongolic people and Amerindians.

Having a lot of antigens isn't always better for your health. Just as A antigens can make your blood clot, being positive for Lewis antigens (http://en.wikipedia.org/wiki/Lewis_antigen_system) makes people at extremely high risk for stomach ulcers.

Likewise, the absence of Duffy antigen (http://en.wikipedia.org/wiki/Duffy_antigen_system) is protective against malaria. Once again, humans have been shown to be close to other primates, as baboons have evolved the same Duffy antigen immunity (http://spittoon.23andme.com/2009/06/24/malaria-has-driven-evolution-in-humans-and-baboons-alike/) as the one found in humans.

Nomacomoro
04-09-10, 14:06
Thank you very much for such usefull information

Aristander
05-09-10, 04:42
Thanks again for the great information! :good_job:

Carlitos
05-09-10, 19:16
Thank you very much for such usefull information. I´m AB+

Maciamo
26-10-10, 13:23
According to a new study (http://www.newscientist.com/blogs/shortsharpscience/2010/10/-normal-0-false-false-3.html?DCMP=OTC-rss&nsref=online-news), blood type O are twice as likely as type A or AB women to have a reduced egg count. Blood group O may therefore have a negative incidence on female fertility.

Most of the women in my family are A, while most of the men are O. I wonder if Nature (i.e. genetics) makes it more likely for women to inherit from a blood type increasing female fertility. It would make sense from an evolutionary point of view. Men would benefit more from being O, as it reduces the risk of cardio-vascular problems, more common in males than females. Unfortunately I wasn't able to find blood type statistics by gender to confirm whether there was a difference incidence of each group between men and women.

LeBrok
23-02-11, 18:05
Negative is fine, positive can cause issues with a second child.

Browns44
02-03-11, 06:27
La Brok,
help me understand what you mean by "positive can cause issues with a second child".

thanks

Maciamo
02-03-11, 12:51
Negative is fine, positive can cause issues with a second child.

I think you meant the opposite. Most people are Rh+, but if either the mother or baby happen to be Rh- there is a risk of alloimmune reaction from the mother's body, which can cause hemolytic disease of the newborn (http://en.wikipedia.org/wiki/Hemolytic_disease_of_the_newborn).

LeBrok
02-03-11, 18:06
Lol, I should avoid short thoughts without context. I'm not sure what I meant by myself after few days. :) Possibly I meant a child.

Baby Rh+, Mother Rh+, = no problem
Baby Rh-, Mother Rh- = no problem
Baby Rh-, Mother Rh+ = no problem
Baby Rh+, Mother Rh- = problem

If Baby is Rh+ it means that baby is producing Rh protein, and it flows in the blood. If Mother is Rh- it means she doesn't have Rh protein in her blood. In this case, after a while (by a second child) mother starts producing antibodies to fight kid's Rh protein. Mother immunological system considers Rh protein as a foreign body and destroys them. When this happens the child can dye.

Nasturtium
03-10-11, 14:58
All sources say that the risk for Rh incompatibility between Rh- mom and Rh+ fetus occurs in second pregnancies. The sources indicate that the mother builds up the antibodies after delivery of the first incompatible child and generally only affects subsequent pregnancies. I just have to wonder though: why is that and could there be more subtle effects for the first child? Could a hostile womb environment be affecting gene expression for the first fetus?

My husband and I are both Rh+, but both of our mom's are Rh-. Neither of us have any brother's or sisters (I guess a testament why Rh- is only 15% where it's common!). Our son is autistic and ASD/ADHD/mood disorders do run in our families. Recent studies are indicating that epigenetic changes which affect gene expression via methylation may play a significant role in neuropsychiatric disorders. Does anyone think that Rh incompatibility could be playing a role in methylation, even for the first child? Also, could the apparent rise in some neuropsychiatric disorders be partly caused by medical interventions that increase survivability, and fertility, for Rh incompatible birth outcomes? In a sense, creating more Rh- carriers?


Thanks.

LeBrok
06-10-11, 07:33
These are big dilemmas Nasturtium. I don't thing anyone can give you a definitive answers to your questions. You need a serious scientific research with statistics to prove or disprove the mentioned correlations.
Good luck in your quest.

Algernon
13-10-12, 16:07
Thanks for sharing.

firetown
09-09-16, 13:42
Thanks for the post that brought me here. :)
In addition we have completed last year a study indicating high incidence of health differences between rh negative homozygotes, rh positive heterozygotes and rh positive homozygotes.
I cannot link here yet, but it's on Plos titled "Worse Health Status and Higher Incidence of Health Disorders in Rhesus Negative Subjects".

There are also studies indicating strong differences in frequencies when it comes to mental health issues and behaviour.
A people are more likely to commit suicide, develop OCD and high stress levels often worsen their overall health.

O and B are more likely to commit murder for example.

There is definitely a connection between physical and mental health. And with mental health come personality traits.

There are plenty of more studies regarding schizophrenia, manic depression and so on.
It's true that there is no ideal blood type to deal best with today's world. But it is important IMO to be aware of our blood type, what comes with it and how it can help us avoid suffering any type of illnesses we are most prone to.

Goga
04-12-16, 21:19
My blood type is A+ (like that of my father, I guess). The blood type of my mother is O-. Her first born son (would be my older brother) was born death. I'm her second child and I was born premature and I was also a very sick baby (it is a miracle that I'm now 100% healthy).

Goga
04-12-16, 21:34
There are also non ABO blood groups.

According to 23andme I'm:


Di(a-b+)

" Immune responses to blood mismatched for the Diego blood group can cause moderate to severe transfusion reactions and mild to severe hemolytic disease of the newborn.

The Diego blood group is interesting to anthropologists because the distribution of the various blood types is different in diverse populations from around the world. The Di(a) version of this blood group is mainly found in populations of Mongolian descent. It is found in 36% of South American Indians, 12% of Japanese, and 12% of Chinese, but is rare in Caucasians and Blacks (0.01%). Interestingly, the Di(a) antigen is less rare in the Polish population (0.47%) compared to most Caucasian populations (0.01%). This may reflect the invasion of Poland by Tatars (who have Mongolian heritage) many centuries ago. The Di(b) blood group antigen is found in almost every population.


Frequencies of the Diego blood types:
Di(a-b+) is found in more than 99.9% of Europeans and Africans and >90% of Asians.
Di(a+b+) found in less than 0.1% of Europeans and Africans and in 10% of Asians.
Di(a+b-) found in less than 0.01% of Europeans, Africans, and Asians. "


K-k+
Kp(a-b+)

" Immune responses to blood mismatched for the Kell blood group can cause severe transfusion reactions and severe hemolytic disease of the newborn (reactions against K are stronger than against k, Kpa, or Kpb). In the case of hemolytic disease of the newborn, the mother's antibodies prevent red blood cells from being made in the fetus.

The k version of this blood group antigen is much more common than the K version in most populations. The K-k+ blood type is found in 98% of Africans and 91% of people of European ancestry. Twenty-five percent of people with Arabic ancestry have the K version on their red blood cells. The Kp(a-b+) blood type is found in 97.7% of Europeans and 100% of Africans. "


Jk(a+b+)

" Immune responses to mismatched blood for the Kidd blood group can cause moderate transfusion reactions and mild hemolytic disease of the newborn. In fact, the reactions are so mild that antibodies against Kidd blood group antigens can be difficult to detect when a doctor does a cross-matching test, so transfusion reactions due to Kidd group mismatches end up happening more often than with other blood groups.

It's possible not to have Kidd blood group antigens on your red blood cells due to a genetic change for which 23andMe does not report data. This genetic change is very rare and occurs only in people with Polynesian and Finnish ancestry.

Frequencies of Kidd blood types:
Jk(a+b+): 50% Europeans, 41% Africans, 49% Asians
Jk(a+b-): 26% Europeans, 51% Africans, 23% Asians
Jk(a-b+): 23% Europeans, 8% Africans, 27% Asians "

Goga
04-12-16, 21:40
Any other reason than 'Mongoloid' ancestry in Poland why they have more 'Mongoloid Di(a) antigen (due to Tatar invasions) than most 'Caucasoid' populations??

8260


http://i.imgur.com/SVjFT7s.jpg
23andme.com

firetown
06-12-16, 07:56
These are big dilemmas Nasturtium. I don't thing anyone can give you a definitive answers to your questions. You need a serious scientific research with statistics to prove or disprove the mentioned correlations.
Good luck in your quest.

I have spent the past 7 years researching this. In part it was digging up research that already existed, but was hard to find. Unfortunately 9 out of 10 Google results about the rh negative blood factor are from sites claiming that rh negative blood comes from aliens and reptilians and I blame for the most part the idiotic public for reacting so favorably towards nonsense overlooking simple scientific facts I am about to lay out. You will also when researching realize that there is financial interest not to educated people properly as policies in place actually not only ensure a generation of sick children of rh negative mothers, but also that the autism epidemy likely stems from those policies. Remember: The anti D shot for rh negative mothers became available in 1968. When exactly did the autism epidemy begin? ...

And where has it hit? Do you think it is coincidence that this epidemy happened in the countries where policy dictates to give the anti D shot DURING the pregnancy rather than before or after?

The damages done within the fetus happen twofold:
1) Before the anti D shot, a fetus would just die being destroyed by the antibodies with no chance of survival. Now when the mom has antibodies, the fetus is unprotected allowing the anitbodies to eat up its brain cells which literally happens. Then rather than letting nature have its way, the saving shot keeps the damaged fetus alive.
2) Aluminum and mercury interchangably had been ingredients in the shot which are bad enough for a mother but imagine those particles entering a tiny fetus ...


All sources say that the risk for Rh incompatibility between Rh- mom and Rh+ fetus occurs in second pregnancies. The sources indicate that the mother builds up the antibodies after delivery of the first incompatible child and generally only affects subsequent pregnancies. I just have to wonder though: why is that and could there be more subtle effects for the first child? Could a hostile womb environment be affecting gene expression for the first fetus?

My husband and I are both Rh+, but both of our mom's are Rh-. Neither of us have any brother's or sisters (I guess a testament why Rh- is only 15% where it's common!). Our son is autistic and ASD/ADHD/mood disorders do run in our families. Recent studies are indicating that epigenetic changes which affect gene expression via methylation may play a significant role in neuropsychiatric disorders. Does anyone think that Rh incompatibility could be playing a role in methylation, even for the first child? Also, could the apparent rise in some neuropsychiatric disorders be partly caused by medical interventions that increase survivability, and fertility, for Rh incompatible birth outcomes? In a sense, creating more Rh- carriers?


Thanks.

I will go one by one on those and in the end link to my site where all of it is referenced in various places depending on the many subjects you are addressing.



All sources say that the risk for Rh incompatibility between Rh- mom and Rh+ fetus occurs in second pregnancies. The sources indicate that the mother builds up the antibodies after delivery of the first incompatible child and generally only affects subsequent pregnancies. I just have to wonder though: why is that and could there be more subtle effects for the first child? Could a hostile womb environment be affecting gene expression for the first fetus?

Chemical pregnancies are a phenomenon I have only seen in rh negative women. Then the amount of miscarriages before a first pregnancy being sky high in rh negative women .... all of those are indicators, very strong ones, that you suspicion is 100 percent correct and again dictates that all rh negative women need to have the shot BEFORE the first pregnancy, IF and ONLY IF their partners are rh positive. Of course, hospital lawyers will advise that having rh negative partners does not keep a woman from cheating, but the if and only if rule is the only feasible protecting you and your offspring from unnecessary injections and ensuring you get the injection if and WHEN you need it.



My husband and I are both Rh+, but both of our mom's are Rh-.

If your rh negative mothers have mothers who are rh positive, then likely they are born with the antibodies. just like the rh negative mom and the rh positive fetus connect via placenta interchanging blood, so do rh positive moms with the rh negative fetus ensuring that the rh negative baby is born with already developing antibodies, so a first pregnany with an rh positive baby will already affect the fetus.


Neither of us have any brother's or sisters (I guess a testament why Rh- is only 15% where it's common!). Our son is autistic and ASD/ADHD/mood disorders do run in our families. Recent studies are indicating that epigenetic changes which affect gene expression via methylation may play a significant role in neuropsychiatric disorders. Does anyone think that Rh incompatibility could be playing a role in methylation, even for the first child?

Yes, as stated above and also a lot more information I have written partially about, but will have to get back at a later time as it is incomplete and not yet ready to publish. SOrry about it, but I need to ensure every piece is backed by actual data to ensure it sticks.


Also, could the apparent rise in some neuropsychiatric disorders be partly caused by medical interventions that increase survivability, and fertility, for Rh incompatible birth outcomes? In a sense, creating more Rh- carriers?

Nature has its way of protecting "its own" and one thing to mention is a higher sex drive amongst rh negative women being proven, alongside the heterozygotes doing better than rh negatives and also rh positive homozygotes.

Your question is the best I have ever seen at any forum, including my own except one from a lady that has caused me to start this research many years ago.

For anyone critical of my post and rather listening to their doctor, I will link to a post of mine showing how wrong doctors can be and even brag online about knowledge which is wrong. Sadly, the policies in place are against rh negative mothers and doctors in general miseducated and unless they have a special interest in either the subject matter or your well being, their actions are quite likely harmful ( see: can you trust your doctor's judgement? (http://www.rhesusnegative.net/staynegative/can-trust-doctor/))

I see this post of yours is 4 years old, so I am not sure if you are still around. But if you have any follow up questions, please bring them as I would love to use this particular thread to gain additional visibility for issues that should be addressed a lot more and need to be brought to the attention of every single rh negative woman out there planning to ever have children.

~ Mike Dammann

wlaett
17-03-17, 00:27
Interestingly, 23andme said my mother is Diego(a+b+) - which as you note is practically non-existent in populations that do not have at least some Mongolian/Siberian ancestry. In fact several studies have called it useful as a racial indicator. Now, we DID have a very small percentage DNA attributed on her report to the Yakut population of north Siberia, and HAVE had Eurasian features show up in the Estonian line of our family. Estonians and Finns - we're part Finnish on that Estonian line - have more on average genetically in common with east Asians than western and central Europeans, so maybe that is why. I also have strange names like Tudaka turn up in the family (my 9th and 8th Estonian Great Grandfathers on my mother's side were both named Tudaka) and turns out I can only find this as a surname today...in Mongolia.

But as far as me, I don't know - I think my blood TYPE was B+ if I remember my days of donating to the red cross, but I can't seem to find out how the diego (a+b+) is passed down - if my mother is diego(a+b+), what are the odds I - her son - also am? I don't understand that. No idea what my father was, though his side claims to be part native American and I've only found distant cousins so far (a few times removed) who were native- other than that he should be French, Polish and /or Russian and Baltic (Estonia, Latvia, and Lithuania) on his maternal side. That probably increases the odds of him also being diego (a+b+) but as it is VERY rare among even Polish people that seem unlikely.

Guess I'll have to pay $100 to find out my group even though I know our family tree going back 500+years on some lines! :( Wish there were a way to tell my likelihood of being also diego(a+b+) if my mother is without paying money!

Maciamo
17-03-17, 08:01
Interestingly, 23andme said my mother is Diego(a+b+) - which as you note is practically non-existent in populations that do not have at least some Mongolian/Siberian ancestry. In fact several studies have called it useful as a racial indicator. Now, we DID have a very small percentage DNA attributed on her report to the Yakut population of north Siberia, and HAVE had Eurasian features show up in the Estonian line of our family. Estonians and Finns - we're part Finnish on that Estonian line - have more on average genetically in common with east Asians than western and central Europeans, so maybe that is why. I also have strange names like Tudaka turn up in the family (my 9th and 8th Estonian Great Grandfathers on my mother's side were both named Tudaka) and turns out I can only find this as a surname today...in Mongolia.

But as far as me, I don't know - I think my blood TYPE was B+ if I remember my days of donating to the red cross, but I can't seem to find out how the diego (a+b+) is passed down - if my mother is diego(a+b+), what are the odds I - her son - also am? I don't understand that. No idea what my father was, though his side claims to be part native American and I've only found distant cousins so far (a few times removed) who were native- other than that he should be French, Polish and /or Russian and Baltic (Estonia, Latvia, and Lithuania) on his maternal side. That probably increases the odds of him also being diego (a+b+) but as it is VERY rare among even Polish people that seem unlikely.

Guess I'll have to pay $100 to find out my group even though I know our family tree going back 500+years on some lines! :( Wish there were a way to tell my likelihood of being also diego(a+b+) if my mother is without paying money!


Diego a+b+ indeed comes from Northeast Asian populations and was brought to Europe by various people like the Uralic speakers, Huns and Mongols. In your case the former is much more likely.

You don't need to waste $100 to test your ABO blood type as it is tested b 23andMe. For odd reasons it is not part of the main Trait report but you can find it in the Health Tools, just under Traits in the top menu. You'd better hurry though as 23andMe plans to retire the Health Tools in a few days. If it's too late, you can still check manually these SNP's in SNPedia by adding the odds for each of them: rs8176719 (http://snpedia.com/index.php/rs8176719), rs1053878, rs7853989, rs8176740, rs8176743, rs8176746, rs41302905, rs8176747, i4000504, rs8176749, i4000505.

wlaett
17-03-17, 20:42
Well that's the problem - I wasn't the one who got sequenced - it was my mother - and she's just told me they no longer show her that information for some reason. Seems then like it'd be a waste to have it done for me in order to find out my blood group (as opposed to the normal ABO blood type - which for me I'm fairly confident is B+ or B- if I recall - something B). Seems they've already retired the health tools from what I'm told.

Since it was my mother who was sequenced and not me, her son (Not sure if gender would matter in blood group antigen inheritance) it seems I can’t ceck any of those SNP’s because there’s no guarantee I’d have inherited them.

Basically, I’m unsure of how the blood group – like diego(a+b+) is passed down from mother to son or daughter. I’m also very curious because from what I’ve read diego a+ can be associated with a hemolytic disease of newborns and my little sister died unexpectedly at about 1 month of age when I was 2 years old. I also have some autoimmunal issues with my skin since birth – namely psoriasis-like dry spots on my forehead, cheeks and the middle of my chest that have been there unless I moisturize like mad since I was a baby – none of my other siblings have them but my nephew has them in the exact same spots. I wonder if my mother’s antigens could cause that if I inherited the a- instead of a+, and even though there’s no way of knowing how she died at this point (it was the 1980’s and they just called it SIDS – sudden infant death syndrome – meaning they don’t know).

Does anybody know how the diego antigens are actually inherited? I’ve tried looking into it and there just seems to be almost no information at all on it – possibly because it is incredibly rare among non-asians and even somewhat rare among Asians. Is it just a 50/50 chance of inheriting the a+ and b+ ? Or if your mother had it does that mean you will too?
I’ve always wondered about the cause of my life-long skin issues and my sister’s sudden death. What if it’s so simple as a mismatch of these bits? My father has a highly similar heritage to my mother – both a lot of Baltic/eastern European ancestry, though, so perhaps the odds of inheriting it are actually higher than for most.

Maciamo
23-03-17, 11:20
Well that's the problem - I wasn't the one who got sequenced - it was my mother - and she's just told me they no longer show her that information for some reason. Seems then like it'd be a waste to have it done for me in order to find out my blood group (as opposed to the normal ABO blood type - which for me I'm fairly confident is B+ or B- if I recall - something B). Seems they've already retired the health tools from what I'm told.

Nothing to worry about. Just scan your 23andMe raw data with Promethease (https://promethease.com/) and you'll know your mother's blood type.


Since it was my mother who was sequenced and not me, her son (Not sure if gender would matter in blood group antigen inheritance) it seems I can’t ceck any of those SNP’s because there’s no guarantee I’d have inherited them.


Then just take the test. Aren't people screened for blood types at birth in Estonia? I thought that was a common practice in all EU countries.


Basically, I’m unsure of how the blood group – like diego(a+b+) is passed down from mother to son or daughter.

If one of your parent is Diego(a+b+) you have 50% chance of inheriting it.


I also have some autoimmunal issues with my skin since birth – namely psoriasis-like dry spots on my forehead, cheeks and the middle of my chest that have been there unless I moisturize like mad since I was a baby – none of my other siblings have them but my nephew has them in the exact same spots. I wonder if my mother’s antigens could cause that if I inherited the a- instead of a+, and even though there’s no way of knowing how she died at this point (it was the 1980’s and they just called it SIDS – sudden infant death syndrome – meaning they don’t know).

Very doubtful Diego antigens are causing this. Psoriasis is linked to some HLA types, not Diego types. I am not aware of Northeast Asians having more skin problems than the rest of the world. On the contrary they tend to have quite healthy skin.

firetown
06-06-17, 10:57
which for me I'm fairly confident is B+ or B- if I recall - something B). Seems they've already retired the health tools from what I'm told.

I’ve always wondered about the cause of my life-long skin issues and my sister’s sudden death. What if it’s so simple as a mismatch of these bits? My father has a highly similar heritage to my mother – both a lot of Baltic/eastern European ancestry, though, so perhaps the odds of inheriting it are actually higher than for most.

I think you should start by finding out your exact ABO and rhesus. Because otherwise it will lead to more speculation. Your mom and sister could have had rhesus incompatibility issues. Just one of many possibilities. Could your skin issues also be allergy related?

Wheal
18-09-17, 17:20
The good... O- is the universal donor. Anyone can receive O- blood. The bad... O- can only receive O- blood. I have one son who is O- and one son 0+ so I have identified family members who are 0- just in case my 0- son needs to receive blood.
https://thebloodconnection.org/about-blood/blood-education/blood-types/o-negative/

firetown
07-11-17, 12:26
There are also indirect roles blood type frequencies can play such as different likelihood of being a secretor and non-secretor.
One example:

non-secretion of blood group antigens is a significant risk factor for gastro-duodenal disease and the RR for non-secretors/secretors was estimated to be 1.9
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3827391/

Björnsson
12-09-19, 07:12
My wife and I are both O+. The best map I've seen of ABO global patterns, shows Atlantic Europe as highly O type, so I question the perception of it being indigenous to pre-Mestizo populations of the Americas before Columbus.

firetown
03-05-20, 20:25
My wife and I are both O+. The best map I've seen of ABO global patterns, shows Atlantic Europe as highly O type, so I question the perception of it being indigenous to pre-Mestizo populations of the Americas before Columbus.

What do you mean by that? Most native tribes of the Americas were likely 100 percent O positive.

miamelano
18-10-20, 00:01
The molecular basis of the ABO blood group system was elucidated in 1990. The gene encodes a glycosyltransferase, which transfers N-acetyl D-galactosamine (group A) or D-galactose (group B) to the nonreducing ends of glycans on glycoproteins and glycolipids. The group O phenotype results from inactivation of the A1 glycosyltransferase gene, and the nonreducing ends of the corresponding glycans in group O subjects express the blood group H antigen . The ABH antigens are not confined to red cells but are widely expressed in body fluids and tissues. The biologic significance of the A/B transferase has not been clearly demonstrated, but it would be expected that loss of this functional protein in group O patients would have some deleterious consequences for patients of this blood type.

ructure of ABO and H antigens on human red cells. H antigen formed by the action of FUT1
on oligosaccharide precursor chains in which the terminal D-galactose residue is linked to carbon 4 of the penultimate N
-acetyl D-glucosamine residue (type II chain). (B) Structure of Le blood group antigens in bodily secretions. Secretor gene (FUT2
) regulates the production of H antigen, which can be converted to A or B antigen if the corresponding active ABO glycosyltransferase is present. The ABH, Leb
-active structures are formed on oligosaccharide precursor chains in which the terminal D-galactose residue is linked to carbon 3 of the penultimate N
-acetyl D-glucosamine residue (type I chain) If FUT 2
is deficient the Lea
active structure predominates.

ThirdTerm
21-10-20, 23:12
Blood type O may offer some protection against COVID-19 infection, according to a Danish study. Among the COVID-19 positive, Barnkob et al. (2020) found that people with blood types A, B, or AB may be more likely to be infected with COVID-19 than people with type O, while they did not find any significant difference in rate of infection between A, B, and AB types.

https://i.postimg.cc/x1vrgMPx/advancesadv2020002657absf1.png

Abstract
Identification of risk factors for contracting and developing serious illness following infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is of paramount interest. Here, we performed a retrospective cohort analysis of all Danish individuals tested for SARS-CoV-2 between 27 February 2020 and 30 July 2020, with a known ABO and RhD blood group, to determine the influence of common blood groups on virus susceptibility. Distribution of blood groups was compared with data from nontested individuals. Participants (29% of whom were male) included 473 654 individuals tested for SARS-CoV-2 using real-time polymerase chain reaction (7422 positive and 466 232 negative) and 2 204 742 nontested individuals, accounting for ∼38% of the total Danish population. Hospitalization and death from COVID-19, age, cardiovascular comorbidities, and job status were also collected for confirmed infected cases. ABO blood groups varied significantly between patients and the reference group, with only 38.41% (95% confidence interval [CI], 37.30-39.50) of the patients belonging to blood group O compared with 41.70% (95% CI, 41.60-41.80) in the controls, corresponding to a relative risk of 0.87 (95% CI, 0.83-0.91) for acquiring COVID-19. This study identifies ABO blood group as a risk factor for SARS-CoV-2 infection but not for hospitalization or death from COVID-19.


“Reduced prevalence of SARS-CoV-2 infection in ABO blood group O” by Mike Bogetofte Barnkob, Anton Pottegård, Henrik Støvring, Thure Mors Haunstrup, Keld Homburg, Rune Larsen, Morten Bagge Hansen, Kjell Titlestad, Bitten Aagaard, Bjarne Kuno Møller and Torben Barington, 14 October 2020, Blood Advances.
DOI: 10.1182/bloodadvances.2020002657


https://ashpublications.org/bloodadvances/article/4/20/4990/463793/Reduced-prevalence-of-SARS-CoV-2-infection-in-ABO

miamelano
15-11-20, 21:50
The molecular basis of the ABO blood group system was elucidated in 1990. The gene encodes a glycosyltransferase, which transfers N-acetyl D-galactosamine (group A) or D-galactose
michaeldadson.com(group B) to the nonreducing ends of glycans on glycoproteins and glycolipids. The group O phenotype results from inactivation of the A1 glycosyltransferase gene, and the nonreducing
ends of the corresponding glycans in group O
subjects express the blood group H antigen .
michaeldadson.info The ABH antigens are not confined to red cells but are widely expressed in body fluids and tissues. The biologic significance of the A/B .gentlecurrentstherapy.com/michael-dadson-clinical-counsellor transferase has not been clearly demonstrated, but it would be expected that loss of this functional protein in group O patients would have some deleterious consequences for patients of this blood type.


ructure of ABO and H antigens on human red cells. H antigen formed by the action of
FUT1
on oligosaccharide precursor chains in which the terminal D-galactose residue is linked to carbon 4 of the penultimate
N
-acetyl D-glucosamine residue (type II chain). (B) Structure of Le blood group antigens in bodily secretions. ecps.educ.ubc.ca/michael-dadson-final-phd-defence-cnps / Secretor gene (
FUT2
) regulates the production of H antigen, which can be converted to A or B antigen if the corresponding active ABO bc-counsellors.org/counsellors/michael-dadson /glycosyltransferase is present. The ABH, Le
b
-active structures are formed on oligosaccharide precursor chains in which the terminal D-galactose residue is linked to carbon 3 of the penultimate
N
-acetyl D-glucosamine residue (type I chain) If
FUT 2
is deficient twitter.com/dadsonmichael the Le
a
active structure predominates.
It is of crucial importance to identify risk factors for contracting and
developing serious illness after infection with extreme acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
In order to determine the effect of common blood groups on the susceptibility of viruses, we conducted a retrospective cohort study of

all Danish individuals screened for SARS-CoV-2 between 27 February 2020 and 30 July 2020 with a documented ABO and RhD blood group.
Blood group distribution was contrasted

with data from nontested individuals.
Participants (29% of whom were male) included 473 654 individuals tested with real-time polymerase chain reaction for SARS-CoV-2 (7422

positive and 466 232 negative) and 2 204 742 nontested individuals, representing approximately 38% of the total Danish population.
For confirmed infected cases, hospitalization and death from COVID-19,

age, cardiovascular comorbidity, and job status were also collected.
ABO blood groups ranged substantially between patients and the reference group, with just 38.41% (95% confidence interval [CI], 37.30-39.50) of blood group O

patients compared to 41.70% (95% CI, 41.60-41.80) of control patients, leading to a relative risk of 0.87 (95% CI, 0.83-0.91) for COVID-19 acquisition.
This research identifies the ABO blood group as a risk factor

for infection with SARS-CoV-2, but not for COVID-19 hospitalization or death.

firetown
16-11-20, 09:37
Another study examines a possibility that likelihood of transmission depends on blood type compatibility:

Several independent datasets suggest blood type A is over-represented and type O under24 represented among COVID-19 patients. Here, I model a scenario in which ABO transfusion incompatibility reduces the chance of a patient transmitting the virus to an incompatible recipient. Comparison of model outputs to published data on COVID-19 prevalence indicates that if this scenario holds true, ABO incompatibility may reduce virus transmissibility by 60% or more. Paradoxically, however, targeted vaccination of either high-susceptibility type A or “super spreader” type O individuals is less effective than random vaccination at blocking community spread of the virus. Instead, the key is to maintain blood type diversity amongst the remaining susceptible individuals. I stress that these results illustrate a theoretical model of ABO blood group interaction with virus transmission and require confirmation by observation.



https://www.rhesusnegative.net/staynegative/2020-07-13-20152637v2-full/

It suggests:

AB>A>B>O

This primarily depends on frequencies of blood types compatible to transmit easiest.

Northener
17-11-20, 20:52
Blood type O may offer some protection against COVID-19 infection, according to a Danish study. Among the COVID-19 positive, Barnkob et al. (2020) found that people with blood types A, B, or AB may be more likely to be infected with COVID-19 than people with type O, while they did not find any significant difference in rate of infection between A, B, and AB types.

https://i.postimg.cc/x1vrgMPx/advancesadv2020002657absf1.png

Abstract
Identification of risk factors for contracting and developing serious illness following infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is of paramount interest. Here, we performed a retrospective cohort analysis of all Danish individuals tested for SARS-CoV-2 between 27 February 2020 and 30 July 2020, with a known ABO and RhD blood group, to determine the influence of common blood groups on virus susceptibility. Distribution of blood groups was compared with data from nontested individuals. Participants (29% of whom were male) included 473 654 individuals tested for SARS-CoV-2 using real-time polymerase chain reaction (7422 positive and 466 232 negative) and 2 204 742 nontested individuals, accounting for ∼38% of the total Danish population. Hospitalization and death from COVID-19, age, cardiovascular comorbidities, and job status were also collected for confirmed infected cases. ABO blood groups varied significantly between patients and the reference group, with only 38.41% (95% confidence interval [CI], 37.30-39.50) of the patients belonging to blood group O compared with 41.70% (95% CI, 41.60-41.80) in the controls, corresponding to a relative risk of 0.87 (95% CI, 0.83-0.91) for acquiring COVID-19. This study identifies ABO blood group as a risk factor for SARS-CoV-2 infection but not for hospitalization or death from COVID-19.


“Reduced prevalence of SARS-CoV-2 infection in ABO blood group O” by Mike Bogetofte Barnkob, Anton Pottegård, Henrik Støvring, Thure Mors Haunstrup, Keld Homburg, Rune Larsen, Morten Bagge Hansen, Kjell Titlestad, Bitten Aagaard, Bjarne Kuno Møller and Torben Barington, 14 October 2020, Blood Advances.
DOI: 10.1182/bloodadvances.2020002657


https://ashpublications.org/bloodadvances/article/4/20/4990/463793/Reduced-prevalence-of-SARS-CoV-2-infection-in-ABO

There are always exceptions to the 'rule' my wife has had corona and has O+ and I 'escaped' the disease with A- ;)

firetown
17-11-20, 21:08
There are always exceptions to the 'rule' my wife has had corona and has O+ and I 'escaped' the disease with A- ;)
Interesting. It is definitely harder for Rh negatives to catch. There are several studies out now all showing this in their results.