The study is here:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7354354/
The conclusion reads:
Blood type is not associated with risk of progression to severe disease requiring intubation or causing death, nor is it associated with higher peak levels of inflammatory markers. Patients with blood types B and AB who received a test were more likely to test positive as were those who are Rh+ positive, and blood type O was less likely to test positive.
This part highlights the blood type A discrepancies with previous studies:
Blood type O had the lowest frequency of disease positivity, similar to Zhao et al., but blood type A had a lower frequency than blood types B and AB [13]. Both Zhao et al. and Zietz and Tatonetti, in their preliminary data, show correlation between blood type A and likelihood of positive testing and blood type O and likelihood of negative testing [13, 14]. The finding related to blood type O appears to correlate across our study and that of both Zhao et al. and Zietz and Tatonetti, but the blood type A correlation was not found in our study [13, 14]. This association of blood type O being less common in infection is the same as that found for SARS-CoV-1 [17]. The Rh+ association with disease positivity appears to be a novel finding and warrants further investigation. Given the relative rarity of rhesus negative blood types, these could not be stratified out by blood type given our patient numbers in this study.
I have bolded the part interesting to those looking for information related to the Rh factor.
This is my video:
See also:
English
Afrikaans
Albanian
Amharic
Arabic
Armenian
Azerbaijani
Basque
Belarusian
Bengali
Bosnian
Bulgarian
Catalan
Cebuano
Chichewa
Chinese (Simplified)
Chinese (Traditional)
Corsican
Croatian
Czech
Danish
Dutch
Esperanto
Estonian
Filipino
Finnish
French
Frisian
Galician
Georgian
German
Greek
Gujarati
Haitian Creole
Hausa
Hawaiian
Hebrew
Hindi
Hmong
Hungarian
Icelandic
Igbo
Indonesian
Irish
Italian
Japanese
Javanese
Kannada
Kazakh
Khmer
Korean
Kurdish (Kurmanji)
Kyrgyz
Lao
Latin
Latvian
Lithuanian
Luxembourgish
Macedonian
Malagasy
Malay
Malayalam
Maltese
Maori
Marathi
Mongolian
Myanmar (Burmese)
Nepali
Norwegian
Pashto
Persian
Polish
Portuguese
Punjabi
Romanian
Russian
Samoan
Scottish Gaelic
Serbian
Sesotho
Shona
Sindhi
Sinhala
Slovak
Slovenian
Somali
Spanish
Sudanese
Swahili
Swedish
Tajik
Tamil
Telugu
Thai
Turkish
Ukrainian
Urdu
Uzbek
Vietnamese
Welsh
Xhosa
Yiddish
Yoruba
Zulu
There is no mention of blood type A+ or A-.
I am A negative. Does this mean I am at more or less risk?
According to this study, neither, but previous other studies have indicated higher risk.
“Blood type and outcomes in patients with COVID-19”
interesting…i’m using this link to the data: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7354354/pdf/277_2020_Article_4169.pdf
“Abstract
This study aimed to determine if there is an association between ABO blood type and severity of COVID-19 defined by intubation or death as well as ascertain if there is variability in testing positive for COVID-19 between blood types. In a multi-institutional study, all adult patients who tested positive for COVID-19 across five hospitals were identified and included from March 6th to April 16th, 2020.Hospitalization, intubation, and death were evaluated for association with blood type.” … “During the study period, there were 7648 patients who received COVID-19 testing throughout the institutions. Of these, 1289 tested positive with a known blood type. A total of 484 (37.5%) were admitted to hospital, 123 (9.5%) were admitted to the ICU, 108(8.4%) were intubated, 3 (0.2%) required ECMO, and 89 (6.9%) died. Of the 1289 patients who tested positive, 440 (34.2%) were blood type A, 201 (15.6%) were blood type B, 61 (4.7%) were blood type AB, and 587 (45.5%) were blood type O. On univariate analysis, there was no association between blood type and any of the peak inflammatory markers”
– some of my comments…i’m looking at the data and making my own conclusions – i’ll be comparing this study to the NYC one here: https://www.rhesusnegative.net/staynegative/protective-associations-between-rh-negative-blood-groups-and-sars-cov-2-infection-and-death/#comment-11035
both studies likely gathered their data from roughly the same time period, when the positivity rates were highest for each city: Boston vs. New York City (March – April 2020). Boston had gave 7648 CVD19 tests & NYC 7700…Boston had 1289 that tested positive with a known blood type, while NYC had 2206 total positive cases. this new study (Boston) claims no difference in severity based on Rh(D) neg/pos status, whereas the NYC study showed a significant difference that favored Rh(D) negs w/ less intubation and lower death rates.
similar factors that are apparently associated w/ positive CVD19 status for both studies are: hypertension, cardiovascular diseases, respiratory diseases, diabetes mellitus and obesity…while Boston also noted that roughly 20% were smokers. both studies showed more women apparently tested positive, at a rate of basically 60% or a a little higher for Boston. slightly more than 50% claimed to be non-white & positive in NYC, while 553 or ~ 43% were white & positive in Boston. this does seem to show a higher positivity occurrence in non-whites generally (i think in both studies the % of whites in the general population should be noticeably higher than the #’s / %’s given as positive cases for them in these 2 studies).
an overarching question for both studies (for us) is what is the percentage of Rh(D) negs in the general population for each area? for NYC it is likely somewhere between 9% and 14% (as noted in my post) and in that case study the Rh(D) negs were less likely to test positive and much less likely to have severe outcomes. regarding the Boston study: i didn’t see any Rh(D) neg estimates given. i made a search and found this OB/GYN Boston based company giving/using #’s for the USA as a whole of 16% for the prevalence of Rh(D) blood type: https://bfobgyn.com/health-library/healthwise/?DOCHWID=hw3681 … so, given my understanding of the type (racial & ethnicity) of the people who make up the general population of Boston: i suspect the % of Rh negs would be even higher than those for NYC overall. i’ll perhaps be conservative and give Boston an Rh(D) neg range of somewhere around 12%. in the Boston study: 1161 tested positive & were also Rh(D) positive. of the 1289 total positive cases, these Rh(D) positive people are 90% of that total. this means the Rh(D) negs were 10% of the total positive CVD19 group. so that likely means the Rh(D) negs were perhaps 20% or more less likely to test positive given my estimate of the prevalence of Rh(D) negs in the gen’ pop’ of Boston.
in the Boston study: the % intubated was lowest for blood group B and the % that died was lowest for blood group O. so once again, most of the noticed trends/traits for Rh(D) neg blood seem present here. once again: given what i think is the general racial/ethnic make up of the Boston area, i think whites once again were not as much affected as were others. this study apparently did see something like that in the data also: “A final element worthy of discussion is that there is certainly a racial element to ABO blood typing [20]. We were able to account for confounding factors of race and primary language through our multivariable models, likely isolating the effect of ABO blood typing, independent of ethnicity. However, the full effects of ethnicity on COVID-19 susceptibility and severity warrant further investigation.”
Thank you so much, Ken. Just one quick comment before I read more on it:
“ethnicity”
I disconnect from that term or the term “race”.
It is a box for idiots.
This is for those who will read this who have not yet participated in commenting.
There is more:
Ethnicity is something that is based on ancestry, but in terms of terminology, it has becomes a push into one of 5 boxes.
It seems people try to demand a push. Ancestry is not about skin color, but common ancestry. Since this is really sickening in terms of the feeling I get “explaining the obvious”, I will stop right here.
Thank you again, Ken!
i keep bringing up the “racial”/”ethnic” & “white” stats in these studies, if they use them, because i do believe and think the CCR5-delta32 mutation is likely having an effect on the results, outcomes & infection rates of “whites” specifically; since the prevalence of this mutation is largely/almost entirely a “white” European & their descendants genetic issue. a mutation that i apparently have.
i am certainly not the only one using these terms (race/ethnic/skin-color terms/words)…words that most people will use in describing the data/results/outcomes/% infected and so on. i think i mentioned more than a month or so here, that in the USA, it has often been stated that people other than “whites”… i.e./that “blacks”. “latinos”, “native americans”, “asians” and so on are apparently suffering more from CVD19 and more often. people still don’t mention often the different strains this virus has or that in NYC there were apparently two strains circulating simultaneously and infecting during the March-April 2020 past peak (data shows some were infected w/ both the original strain from China and a more virulent one/the European strain concurrently…and thus, seemingly w/ compounding effects and more deaths). i’d rather talk about specifics, genetics, alleles, mutations (and perhaps i will)…but, unfortunately most won’t. “white” skin is genetic w/ few exceptions, as is being Rh(D) neg and so on…some are intolerant of differences….some want all to be the same…i want to know what’s going on and what the differences actually mean/what’s their significance. i think i know some things, but i also know there’s still much to learn. i won’t learn a damn thing w/out studying, integrity and well-focused persistent effort. so as i like to say: success to those & that which are good…and best wishes to the large, extended and diverse Rh(D) neg family.
i was just looking at the data again here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7354354/pdf/277_2020_Article_4169.pdf
specifically the data in table 4: and i noticed that out of the 1289 total positive CVD19 case, 1167 were Rh(D) positive which is approximately 90.54% of the total confirmed positive test results…which means there were 128 Rh(D) negs who tested positive out of the 1289 total positive CVD19 cases, for roughly 9.93% of that total. if, the Boston population has maybe 16% Rh(D) negs (which i think is a possibility given the #’s from this Boston based OB/GYN’s website under their “ABO test” section) https://bfobgyn.com/health-library/healthwise/?DOCHWID=hw3681 … then, it’s entirely possible that the percent of Rh(D) negatives in this study represents maybe only ~ 62.06% of their true % prevalence in the general population….or perhaps ~ 37.94% less. that’s very significant if it’s true.
oops, i just noticed some bad math i did in a reply i just submitted: i noticed some percentages added up to more than 100%…so, my mistake was w/ the # of Rh(D) negative…it’s 122 not 128. which means their percentage is ~ 9.46% of the total positives cases and not ~ 9.93%. this also affects the results i posted in this section: then, it’s entirely possible that the percent of Rh(D) negatives in this study represents maybe only ~ 59.125% of their true % prevalence in the general population….or perhaps ~ 40.875% less. that’s very significant if it’s true.
Hi ken,
Thank You for all contributions! Very informative. I read blog, An distressed from my intentional observation as a total ” need to kbow” RH negative Differential. So few of us contributing blood samples. Yes? I’ve watched listened,observed and meditated..then reflected responses. Your deductive…I’m emotional. I worry that RH neggs may assume from miniscule , premature research that they may perhaps be be resistant or immune to virus. I get your reporting facts as facts become available. But I’m on the frontlines…working, and virus is not by any means consistant…The variables have changed and changed…For those not medical, or as smart as you, let’s tell the truth! N 95 masks prevent transmission…all others dont, not really even k95 masks…Do they help? Yes!…so let’s assume we are all able to contract virus. Practice universal precautions always…Studies are premature! We know that this viral name has changed…how many times? Who knows…testing in China on initial virus won’t help now! Event 201 bill gates states 18megs no vaccine, will effect children previously A symptomatic( no symptoms) contagion will be child to parent…so let’s wear n95 masks, obey social distancing, and practice good hygiene??! Then when all give blood and cheek swab, enough, then conclusions can be analized…if an RH neg brother or sister believes there immune without proper long term testing all strains…someone may suffer a loss…let’s research and promote safety first!!! Thanks
Please except my apology. I read fast..missing important facts when I’m tired!. I see clearly what you are researching and suggesting! So Ken our RH neg. Thinking is very much in sync..I have been writing data, observations, I know about the negligent abi!ity to intubate!!! Right now I’m screaming yelling pleading with government to investigate hospitals. It’s long, it’s a small price of the p ie….my plea is that residents and “some” people claiming to have there doctorate be tested and trained clinically prior to emergency situations where it’s just not ok to perforated the esopgagus….I was apples, you were oranges in the co mments…I see what your seeing and it’s deplorable. Regarding our blood types and resistance…well with uneducated children with minimal skills placed in or and insufficient respirators..that blow lungs out, well donating our blood to figure resistance to virus is non essential if proper medical treatment not rendered. My nephew was three, they only had adult reperstor, well he died…lungs blew up..needed pedo…much wrong!!! I’m ashamed I was thinking of my longevity..by way of immunity…so selfish, unaccepptable…forgive me for not reading the entire article…I’m actually not narcissistic, but I feel guilty so maybe I was only worried about my own mortality? Sorry! I hate saying dumb things ect…I am working hard because I walked away from a bad situation….just adjusting, I hate the silence! It’s a process…forgive my divits!!!I’m just learning to be me
we all make mistakes…i do constantly w/ spelling here…less often w/ my thinking ( i am a better thinker than typist : ) … i suggest that you try to learn some patience…maybe try to slow down a little. always try to check your work/typing or whatever here. i check mine, yet some spelling/word context & such errors get past me. i see them after i post my comment for review. so, w/out an edit feature here – i often make some mistakes when posting something complex and/or long. oh well, i’m doing the best i can. got any suggestions for me Robin? maybe i should smile more and maybe be a little more friendly or social huh? it’s good to see Mike’s back at work.
Thank you, Ken. Have you ever tried to register at this blog? Let me know if it is possible. If not, I will see how to do it.
No, you shouldn’t smile more unless you feel like smiling more. I have enough smiling around me, not with eyes, but mouth. I need reality in my life. 🙂
I would love to set you up as a moderator here if that is possible. I need to have comments moderated,,, otherwise it will be flooded with alien propaganda, but I hate to see you and some others being delayed. The forum is another option and I can make the content visible (easy to moderate and set things up), but it is very dead. Not sure what the best option is as this blog is where I have posted studies for years alongside you and some others, so this is the information center at this point.
Thank you Ken ! I went through the same process and came to similar conclusions !
Thank you Mike ! By way of perspective, i find it helpful to remember that the “5 ethnic boxes” issue is a US one. Other countries do not classify in the same way. Europeans for example consider Spaniards as a nationality…not as “Hispanics”.
However, the underlying biological genetics are the same regardless of the layer of culturally imposed confusion…and the studies cited speak to the need for better focused studies that go beyond correlations to well formulated hypotheses about causality and the underlying molecular biology.
Thank you for this information. I’m so glad this is finally getting studied. I have searched a long time for the blood type percentages for each State, with no luck. I think that info could be useful. Do you think rh negatives should get the covid vaccine?(depending on what exactly is it) I hope I don’t start a vaccine argument but I wonder what other rh negatives think about getting a covid vaccine…
each must decide that for themselves i think. each is unique as are their situations. i posted here: https://www.rhesusnegative.net/staynegative/protective-associations-between-rh-negative-blood-groups-and-sars-cov-2-infection-and-death/#comment-11062 … about many things i have and will use if and when CVD19 gets close to me here in NY State again (i mentioned on an earlier topic about how i bought 2 bottles of Don Q 151 proof rum to take a “shot”/or part of a mouth full of it once in a while if i thought i was infected…the idea being that w/ an alcohol content of 75.5% it should likely kill the virus & maybe some other things too as it goes into and through my system/body). some things are/seem to be helpful as preventatives and others are supposedly good for when symptoms begin to develop. do your own research and try to be prepared and ready. this virus is likely going to be here indefinitely…for a long time i think.
– the following demographics should be quite accurate, and may represent current year 2020 estimates or something close to that –
“Boston Demographics
According to the most recent ACS, the racial composition of Boston was:
White: 52.58%
Black or African American: 25.26%
Asian: 9.64%
Other race: 7.06%
Two or more races: 5.10%
Native American: 0.32%
Native Hawaiian or Pacific Islander: 0.04%”
https://worldpopulationreview.com/us-cities/boston-ma-population
“New York Demographics
According to the most recent ACS, the racial composition of New York was:
White: 42.67%
Black or African American: 24.27%
Other race: 15.12%
Asian: 13.95%
Two or more races: 3.51%
Native American: 0.43%
Native Hawaiian or Pacific Islander: 0.05%”
https://worldpopulationreview.com/us-cities/new-york-city-ny-population
– fwiw: 3 of the NYC Presbyterian hospitals (apparently in the NYP/CUIMC study) are outside of the Manhattan/Brooklyn/NYC area. so, this would likely raise the % of whites who used these hospitals above the ~ 43 % they represented in New York City in the #’s i posted above. this requires some speculation on my part surely. i will wait for more good data from other relevant studies and see what i can glean from them. –
https://www.nyp.org/locations
fwiw, i decided to get more accurate and specific about when i got a smallpox shot / supposed vaccination. i thought it was during 1969 (that was for pertussis/whooping cough), but according my records it appears i was given the smallpox shot twice ~ 6 months apart: around my age of ~ 1 1/2+ – 2+ yrs. how many got this shot twice? looks like our family Dr. gave up me w/ this thing after these 2 shots.
to my mother Rh A-, they applied it, but it never caught her.
My brother Rh A-, it was applied in 1974 and the health book says “negative result”
Mike, I agree with you about how lazy thinkers will jump on somebody else’s belief bandwagon so they won’t have to work things out for themselves & also how important that intuition is when formulating your own beliefs. But why is your intuition so more important than mine, when it comes to you discounting my belief system. It’s taken me many years of investigation & using my intuition to arrive at my own beliefs which are constantly evolving. I’m willing to admit that in the future if I receive enough evidence, I’m willing to modify my beliefs because they aren’t set in stone. It seems to me that sometimes poupular belief systems whether secular or scientific thend to act like the inquisition & pass judgment down too quickly on others. I really don’t need to have my beliefs accepted by others, because I have always been a lonewolf. This is a multidimensional universe & there’s room for all of us if we’re willing to admit that all of us are evolving toward the truth and don’t let our egos get in the way.
I got the small pox shot twice ,the reason at he time they said to my parents was because it didn’t take { leave a scar }this was about that time 1969 .. O -neg left handed …thank Mike and Ken for all the info you are sharing I visit the site daily ..
Can anyone clarify, what scientific significance does it have, that the smallpox vaccine has not left a scar? that has not turned on?
for me, my interpretation of a no smallpox scar/”take”: is that the person w/ no scar or “take” (especially after having two shots/vaccinations from different vax batches and maybe at least 6 months later between shots) is already immune to smallpox/the cowpox vaccination somehow. i think it is the CCR5 delts32 gene deletion mutation that gives the no “take” results on children in the US from 1972 or so on backwards (the virus was an extremely serious problem in the past and making quite certain one was vaxed early-on as a child was of the highest level of importance). then, the questions that remains are these: is the CCR5 receptor important regarding CVD19/CoViD-19 and does being heterozygous or homozygous for CCR5 delta32 make any difference w/ respect to CVD19? CVD19, as i understand it affects red blood cells and white blood cells (and other perhaps)…the Rh(D) neg factor is a red blood cell issue, while CCR5 delta32 is affects white blood cells and others cells. so, i would think being hetero’ or homozygous for the delta32 deletion would be quite helpful…seems to me the immune system would be less affected and thus work more as it should to kill CVD19. having cleaner red blood cell surfaces i believe (and have been saying here for a couple month now) is simply put the Rh(D) negative & blood type O benefit against CVD19 as i understand things.
How to spot a cougar at the bar: the vaccine that left a scar – ByTaunya English – October 8, 2015 https://whyy.org/segments/how-to-spot-a-cougar-at-the-bar-the-vaccine-that-left-a-scar/
“The vaccine is a live virus, a cousin of the virus that causes smallpox. That germ creates a small, local infection and nudges the body to mount its defenses. The virus starts multiplying, and within days, the immune system tries to push out the infection.”
Vaccine “Take” Evaluation :: https://www.cdc.gov/smallpox/clinicians/vaccination-take-evaluation4.html
Smallpox Vaccine: The Good, the Bad, and the Ugly :: Clin Med Res. 2003 Apr; 1(2): 87–92. :: doi: 10.3121/cmr.1.2.87 :: Edward A. Belongia, MD and Allison L. Naleway, PhD https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1069029/
“Smallpox vaccine is administered by puncturing the skin multiple times with a bifurcated needle containing a small quantity of vaccine. A small papule develops after 3 to 5 days, following the virus replication in the dermis. The papule evolves into a vesicular and pustular stage over 8 to 10 days. There is typically an indurated area surrounding the central lesion. This is followed by scab formation with development of a residual scar. The process of vesiculation and pustule formation defines a ‘take’ of the vaccine. The take is considered equivocal if a pustule, ulcer, or scab, does not develop at the vaccine site; revaccination is recommended in this situation.”
Vaccine Basics: https://www.cdc.gov/smallpox/vaccine-basics/index.html
Why Does the Smallpox Vaccine Leave a Scar? https://www.healthline.com/health/smallpox-vaccine-scar
Everything you need to know about smallpox vaccine scars
https://www.healthline.com/health/smallpox-vaccine-scar#vs-bcg-with-photo
——————————–
Smallpox In Europe Selected For Genetic Mutation That Confers Resistance To HIV Infection – November 20, 2003 – University Of California – Berkeley https://www.sciencedaily.com/releases/2003/11/031120074728.htm
“The gene produces a receptor, called CCR5, that is the main entry port for HIV-1 into T cells and macrophages. While most people around the world have two CCR5 genes or alleles, about 10 percent of Europeans, on average, lack one of the alleles. They thus produce fewer CCR5 receptors, which hinders initial infection by HIV-1 and slows spread within the body once an immune cell has been infected. Those lacking both alleles produce no CCR5 receptor. ”
“The smallpox virus also has more biological similarities to HIV-1 than does bubonic plague, the authors point out. Plague is a bacterial disease, and there is no evidence that the bacterium, Yersinia pestis, uses the CCR5 receptor in infection. The bacteria actually reproduce outside immune cells.
Smallpox, on the other hand, is a virus based on RNA, just like HIV, she said. And there is some evidence that smallpox, Variola major, uses chemokine receptors like CCR5 to enter cells. ”
“”The Scandinavian countries in particular have very high frequencies of this deletion allele – 14 to 16 percent – which some people have taken to mean that Vikings dispersed the deletion,” Galvani said. “But it could also be due to smallpox hitting Scandinavian countries harder. “”
“”Polymorphisms, the technical term for small differences in peoples’ genomes, are probably often the result of disease, Galvani said. Sometimes they even lead to other diseases, such as the documented case of sickle cell anemia resulting from selection for resistance to malaria.
“There are probably other alleles that have been selected by disease, but we just haven’t found them,” she said. “Diseases have the potential to exert strong selection. There is an arms race between the host to resist and clear infection and the pathogen to evade the resistance. That leads hosts to develop polymorphisms, and then the pathogen to respond by evolving its own polymorphisms, and so on – there is a constant battle.””
————————————
What is CCR5 Delta32?
https://www.delta-32.com/ccr5-delta32.html
“”CCR5-delta32″ is a deletion mutation of a gene which only 1% of the total population has two copies of this gene and individuals who carry two copies of this genetic mutation are immune to Smallpox, The Bubonic Plague (Black Death) and resistant to HIV, the virus that causes AIDS. Up to 20% of the population carry only one copy of this genetic mutation depending on your background and although they still run a significant risk of contracting HIV, the progress of the disease is greatly reduced and can result in a longer life expectancy.””
————————————
CCR5 Δ32 minorallele is associated with susceptibility to SARS-CoV-2 infection and death: An epidemiological investigation :: Clin Chim Acta. 2020 Nov; 510: 60–61. :: Published online 2020 Jul 10. doi: 10.1016/j.cca.2020.07.012 :: Aditya K. Panda https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7347491/
“C-C Chemokine Receptor 5 (CCR5) is an essential member of the G protein-coupled receptor family abundantly present on the surface of monocytes, T cell, and macrophages. CCR5 is known to be responsible for the induction of inflammation in a wide range of infectious diseases and recruit leukocytes towards inflammation sites [2]. The critical role of CCR5 has been elegantly described in a wide range of viral infections: Human Immunodeficiency Virus (HIV), Hepatitis C Virus (HCV) and Hepatitis B Virus (HBV), West Nile Virus (WNV), Tick-Borne Encephalitis Virus (TBEV) [2]. Differential surface expression of CCR5 has been linked with susceptibility/resistance against viral diseases. ”
“”we attempted to address a preliminary question, i.e. “Is the differential infection and mortality rate with COVID-19 worldwide correlated with the distribution of CCR5 Δ32 mutant?””
“These data and findings are indicative of an association of CCR5 Δ32 with susceptibility to SARS-CoV-2 infection and mortality. However, the mechanism of CCR5 Δ32 allele offering predisposition to SARS-CoV-2 infection susceptibility and death of the patient is not known. An earlier investigation on CCR5 deficient mice demonstrated the suppression of Th1 immune response and susceptibility to viral and bacterial infections”
“However, in the present study we observed a positive correlation on 55% of included population, projecting CCR5 Δ32 allele as an important genetic marker of SARS-CoV-2 related death.”
“Although the present report highlighted a significant association of CCR5 Δ32 variant with susceptibility and mortality from SARS-CoV-2 infection, it has set the stage for in-depth analysis by factoring in various other aspects. Inclusion of other genetic polymorphisms of the CCR5 gene can further highlight the role of CCR5 in COVID-19 pathogenesis. ”
————————————
Evaluating plague and smallpox as historical selective pressures for the CCR5-Δ32 HIV-resistance allele
Alison P. Galvani and Montgomery Slatkin
PNAS December 9, 2003 100 (25) 15276-15279; https://doi.org/10.1073/pnas.2435085100 :: https://www.pnas.org/content/100/25/15276.long
“Results
Dominance. Even when we assumed that the resistance allele was dominant, we found that bubonic plague could not generate sufficient selective pressure to account for current CCR5-Δ32 frequencies, despite the periods of unprecedented disease mortality. … However, we found that the more continuous smallpox mortality that afflicted European children since the origin of the allele could have provided the necessary selective pressure to generate the rise of CCR5-Δ32 deletion to current frequencies of 10%”
“Heterozygote fitness is important to the speed of the evolution because most of the selection on the resistance allele occurs via heterozygotes when the frequency of the resistance allele is initially very low.”
“Our results suggest that an origin for the CCR5-Δ32 deletion of 700 years ago is consistent with the allele conferring dominant resistance against smallpox mortality. This would mean that both heterozygotes and resistant homozygotes are fully protected against smallpox mortality (although not necessarily infection). The 95% confidence interval of the 700-year estimate for the origin of the CCR5-Δ32 deletion (275-1,875 years) (16) indicates that the deletion may have arisen earlier. Indeed, another study used the frequency of microsatellite mutations to estimate an age of 1,400. … Under the assumption of incomplete dominance with an additive effect of the resistance allele, case fatality rates of heterozygotes were half those of a susceptible homozygote. That is, the intensity of selection is reduced if dominance is incomplete, requiring more generations of exposure to smallpox epidemics to reach an allele frequency of 10%. ”
“The geographic distribution of the resistance allele also implicates smallpox as the most likely historical source of selection on the CCR5-Δ32 deletion. Although bubonic plague was more intense within central Europe than in Scandinavian populations, the latter were hit particularly hard by intense smallpox epidemics (35). Indeed, the frequency of the CCR5-Δ32 variant forms a north-to-south cline from 0 to 14% across Eurasia (15-18, 36), with greatest prevalence in Scandinavian countries”
————————————
Failure of the Smallpox Vaccine To Develop a Skin Lesion in Vaccinia Virus-Naïve Individuals Is Related to Differences in Antibody Profiles before Vaccination, Not After :: Clin Vaccine Immunol. 2012 Mar; 19(3): 418–428.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294614/
“Successful vaccination against smallpox with conventional vaccinia virus is usually determined by the development of a vesicular skin lesion at the site of vaccinia inoculation, called a “take.” Although previous vaccination is known to be associated with attenuation of the take, the immunology that underlies a no-take in vaccinia-naïve individuals is not well understood. ”
“It is known that previous vaccination against smallpox is associated with an attenuated take upon a revaccination (13, 14). Although the no-take individuals studied here were all vaccinia naive (i.e., they had no exclusion criteria for the clinical trial, such as a vaccination scar or birth date during the eradication campaign), we hypothesized that they had preexisting vaccinia reactivity (or cross-reactivity) of unknown etiology that may be accounting for the attenuated take.”
“DISCUSSION
Successful vaccination against smallpox is conventionally determined by the presence of a take at the site of inoculation. In primary vaccinations, the take involves a 2- to 3-week progression from papule to vesicle, to pustule, to scab (27) but is more rapid, around 8 days, in revaccinations (23). The lesion is thought to be a result of viral damage and inflammation at the site of inoculation (26). In this study, we were able to compare the vaccinia virus-specific antibody profiles of 23 no-takes with naïve and previously vaccinated individuals with a take, both before and after vaccination.”
“The studies described here are presented with this caveat. No-takes that failed to respond are true cases of vaccination failure, for which the skin reaction is a good indicator. This could be due to insufficient dose, problems with vaccine delivery, etc. In contrast, no-take responders are likely to have other underlying reasons for the lack of a take. When these were segregated and compared with the takes, the analyses consistently showed that the profiles after vaccination are essentially identical. This suggests that in no-take responders, the presence or absence of particular antibody responses is not a major determinant in whether a skin take develops.”
“Third, the lack of response to WR132/A13L in ELISA is also consistent with preexisting immunity to orthopox (15). Finally, none of the vaccinees had exclusion criteria indicating previous smallpox vaccination. Overall, the data are consistent with previous exposure to a related orthopoxvirus. We have no information about exposure to other environmental orthopoxviruses by the individuals studied here. However, natural exposure to such viruses may have the same effect as previous smallpox vaccination and contribute to the attenuation of the take.”
“Attenuation of the take may be antibody or T cell mediated. Although we have not measured T cell responses in the this study, we favor the notion that preexisting T cell memory leads to rapid clearance of infection at the site of inoculation and the attenuation of the take without interfering with the boosting effect on the antibody arm of the response. In another study, numbers of residual vaccinia virus-specific CD4+ T cells in individuals vaccinated against smallpox 30 years previously are inversely associated with the size of the skin take upon revaccination (30). Thus, memory T cells remaining after the primary vaccination are likely to contribute to attenuation of the take after revaccination. A similar process may be operating in the vaccinia-naïve no-takes studied here if they were already exposed to a vaccinia virus-like orthopox virus.”
“In contrast, no-takes tend to have higher preexisting antibody titers before vaccination than takes, with profiles not dissimilar to those of previously vaccinated individuals. The origin of these preexisting antibodies is not thought to be vaccinia, but they nevertheless appear to be having an attenuating effect on the take, similar to previous vaccination.”
—————————
Disruption of the CCL5/RANTES-CCR5 Pathway Restores Immune Homeostasis and Reduces Plasma Viral Load in Critical COVID-19 :: doi: https://doi.org/10.1101/2020.05.02.20084673 https://www.medrxiv.org/content/10.1101/2020.05.02.20084673v1
” Here, in 10 terminally-ill, critical COVID-19 patients we report profound elevation of plasma IL-6 and CCL5 (RANTES), decreased CD8+ T cell levels, and SARS-CoV-2 plasma viremia. Following compassionate care treatment with the CCR5 blocking antibody leronlimab, we observed complete CCR5 receptor occupancy on macrophage and T cells, rapid reduction of plasma IL-6, restoration of the CD4/CD8 ratio, and a significant decrease in SARS-CoV-2 plasma viremia. … These results demonstrate a novel approach to resolving unchecked inflammation, restoring immunologic deficiencies, and reducing SARS-CoV-2 plasma viral load via disruption of the CCL5-CCR5 axis, and support randomized clinical trials to assess clinical efficacy of leronlimab-mediated inhibition of CCR5 for COVID-19.”
I haven’t looked much into smallpox before, but there seems to be an associations with blood type AB.
Type O blood group is associated with increased incidence of plague, cholera, mumps, and tuberculosis infections; type A blood group is associated with increased incidence of smallpox and Pseudomonas aeruginosa infection; type B blood group is associated with increased incidence of gonorrhea, tuberculosis, Streptococcus pneumoniae, E. coli, and salmonella infections; and type AB blood group is associated with increased incidence of smallpox, E. coli, and salmonella infections.14 Non-secretors have an increased incidence of Neisseria meningitides, Haemophilus influenza, Candida albicans,14 S. pneumoniae, E. coli urinary tract infections,1 Streptococcus pyogenes, and Vibrio cholerae.24
The same study highlights secretor status in peptic ulcers:
In 1954, it was reported that the incidence of peptic ulcers (gastric and duodenal) was 20% higher for group O individuals than group A individuals, with the incidence of duodenal ulcers 35% higher in group O individuals than in group A, B, and AB individuals, and 50% higher in non-secretors (who make up 20% of the population).
About dengue:
There are no published studies correlating blood groups with zika virus, and only a few for dengue or chikungunya fever;65–69 the findings of one68 are consistent with gene association studies,70 which found that the AB blood group (which lacks antibodies to both A and B antigens) was independently associated with increased susceptibility to severe dengue hemorrhagic fever in secondary infections.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5061611/
– and i became philosophical, which is common for me – yes, differences make a difference…it’s just a matter/question/task of finding out what they are, what they mean/the significance and so on…if one’s interested in doing that of course. the ability to discern differences is directly related to & creates knowledge/intelligence & understanding of things in this world & one’s self upon reflection/consideration/study. if all were the same, all would be one…or perhaps no-thing (a state that’s actually impossible to conceive…thus, all can never be the same). try conceptualizing one whole thing w/out there also being something outside of it/to frame it/define it as a separate thing/an individual – to do so takes/requires a context or something else… like i say: since things exist, things have always existed and always will exist. once again, if one’s interested…what’s going-on/where’s it all going/how’s it all happening and why? each perspective is unique and connected to all else somehow.
Checking the countries, around the world which have populations with a low % of rh- this correlates to the countries with the lowest incidence and mortality rates :
Japan 0.5%
South Korea 0.33%
Taiwan 0.3%
Hong Kong 0.68%
compared to the much higher rh- % in
Belgium 15.0 %
UK 19.0 %
Spain 18.5%
USA 15.0 %
Brazil 19.5%
Thus, ignoring the multitude of other factors – population density, health service quality, equivalent test tracking, etc – surely this points to a high causal alignment
Could somebody please give me more information on CCR5AS, is it helpful against HIV or does it make HIV thrive more easily…
Could somebody please give me more information on CCR5AS, is it helpful against HIV or does it make HIV thrive more easily?