https://www.rhesusnegative.net/staynegative/wp-content/uploads/2020/11/ajh.26019.pdf
Previous reports have documented an association between ABO blood group and risk for infection with the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), the cause of the coronavirus disease 2019 (Covid‐19) pandemic.1–3 Associations between race/ethnicity and SARS‐CoV‐2 positivity have also been reported.4, 5 Here we describe the first large‐scale observational study investigating the associations between ABO group/Rh types with SARS‐CoV‐2 positivity, by major race/ethnicity.
In this retrospective, observational study, test results from a national reference clinical laboratory were assessed to determine the influence of race/ethnicity on the associations of ABO/Rh with SARS‐CoV‐2 RNA positivity. Results from SARS‐CoV‐2 RNA nucleic acid amplification tests (NAAT) performed March through July 2020 were matched with ABO/Rh test results obtained for the same individual since January 2010. Only one SARS‐CoV‐2 result per patient was considered; a patient was considered to have a positive result if any SARS‐CoV‐2 test result was positive. The ABO/Rh testing is generally performed as part of maternal screening; males were excluded. The influence of race/ethnicity on the associations of ABO type/Rh group with SARS CoV‐2 positivity was assessed in a subset of females with available race/ethnicity data.
The SARS‐CoV‐2 RNA NAAT was performed using one of four US Food and Drug Administration (FDA) Emergency Use Authorized tests (Quest Diagnostics SARS‐CoV‐2 RNA [Covid‐19], Qualitative NAAT; Hologic Panther Fusion SARS‐CoV‐2 assay; Roche Diagnostics cobas SARS‐CoV‐2 test; or Hologic Aptima SARS‐CoV‐2 assay). The ABO/Rh typing was performed using solid‐phase technology (Immucor NEO).
Differences in proportions were analyzed using the chi‐square test (with results presented as nominal P values). For multivariable logistic regression models, race/ethnicity was grouped into the following categories: Black non‐Hispanic, Hispanic, white non‐Hispanic, and “other” race/ethnicity (“other” included females of multiple race/ethnicities). Analyses were performed using SAS Studio 3.6 on SAS 9.4 (SAS Institute). This Quest Diagnostics Health Trends study was deemed exempt by the Western Institutional Review Board (Puyallup, Washington).
The study cohort comprised 276 536 females with matched SARS‐CoV‐2 and ABO‐Rh results from all 50 American states and the District of Columbia. There were 34 178 females who were SARS‐CoV‐2 positive (12.4%, 95% CI 12.2%‐12.5%).The median patient age at the time of SARS‐CoV‐2 testing was 34.4 (IQR 29.2‐40.0) years. The SARS‐CoV‐2 positivity rate was higher in both females under 30 years of age (15.1%, 95% CI 14.9%‐15.4%) and those 30‐39 years (11.9%, 95% CI 11.7%‐12.0%) than in females age 40 years or over (10.1%, 95% CI 9.9%‐10.4%) (P < .001 for both comparisons). The most common blood type was O+ (123 642; 44.7%), followed by A+ (83 219; 30.1%); B+ (32 961; 11.9%); O‐ (12 871; 4.7%); A‐ (10 531; 3.8%); AB+ (9048; 3.3%); B‐ (3179; 1.2%); and AB‐ (1085; 0.4%).
The SARS‐CoV‐2 positivity rate was 38% higher in Rh+ patients (12.7%, 95% CI 12.6%‐12.8%) than in Rh‐ patients (9.2%, 95% CI 8.9%‐9.5%) (P < .001). The SARS‐CoV‐2 positivity rate was also significantly higher among type O patients (13.0%, 95% CI 12.8%‐13.2%) than among type A (11.8%, 95% CI 11.6%‐12.0%), type B (11.9%, 95% CI 11.5%‐12.2%), or type AB (11.4%, 95% CI 10.7%‐12.0%) patients (P < .001 for all comparisons). No statistically significant differences in SARS‐CoV‐2 positivity between females with type A and B (P = .66), type A and AB (P = .21), or type B and AB (P = .16) were observed. In stratified analyses, the relationship between SARS‐CoV‐2 positivity and Rh type remained significant across ABO blood groups (Figure S1).
Among the 88 975 females with available race/ethnicity data, the distributions of ABO groups/Rh types were remarkably similar to findings from a large study of blood donors conducted by the American Red Cross.6 In this study SARS‐CoV‐2 positivity rates, as well as ABO/Rh distributions, differed significantly between race/ethnicity groups (Table S1). Hispanic females were significantly more likely to have type O blood (58.3%) than were black non‐Hispanic (49.5%), white‐non‐Hispanic (45.2%), and “other” race/ethnicity females (P < .001 for all comparisons). White non‐Hispanic females were more than twice as likely to be Rh‐ (15.1%) compared to other groups, including “other” race/ethnicity (6.6%), Hispanic (6.4%), and black non‐Hispanic (6.1%) groups (P < .001 for all comparisons). Hispanic females had the highest SARS‐CoV‐2 positivity rate (21.4%, 95% CI 20.9%‐21.9%), followed by black non‐Hispanic (16.3%, 95% CI 15.7%‐16.9%), “other” race/ethnicity (12.8%, 95% CI 12.3%‐13.4%), and white non‐Hispanic (7.2%, 95% CI 6.9%‐7.4%) females.
Unadjusted logistic regression analyses demonstrated similar associations between ABO/Rh variables and SARS‐CoV‐2 positivity in the subset of females with race/ethnicity data as in the overall cohort (Figure 1). However, when race/ethnicity groups were included in an adjusted model, there were two important changes. First, the increased risk of SARS‐CoV‐2 positivity in Rh+ patients fell from 1.44 (95% CI 1.34‐1.54) in the unadjusted model to 1.15 (95% CI 1.06‐1.23) in the adjusted model. Second, the association between type O and SARS‐CoV‐2 positivity changed from being significantly predictive in the unadjusted model (OR 1.07, 95% CI 1.03‐1.11), to significantly protective in the adjusted model (OR 0.95, 95% CI 0.92‐0.99).
This is the largest reported study to date assessing SARS‐CoV‐2 positivity rates by ABO/Rh and race/ethnicity. In line with prior studies,2, 3 our findings demonstrated that Rh positivity, independent of ABO blood group and race/ethnicity, was a statistically significant risk factor for SARS‐CoV‐2 positivity. In contrast to findings from smaller studies,1 our unadjusted analysis showed a significantly higher SARS‐CoV‐2 positivity rate among individuals with type O blood than in those with other blood types. However, after adjusting for race/ethnicity, the relationship between type O and SARS‐CoV‐2 reversed from predictive to protective. Type O and Rh + blood is more prevalent in Hispanics and black non‐Hispanics, two groups in our study with the highest proportions of positive SARS‐CoV‐2 tests. Thus we conclude, in concordance with findings from other studies,1 that type O blood is slightly protective against SARS‐CoV‐2 positivity once race/ethnicity has been considered. The multivariable model also demonstrated that the influence of Rh+ blood type was attenuated when adjusted for race/ethnicity, suggesting that the association between ABO/Rh and SARS‐CoV‐2 positivity is strongly influenced by race/ethnicity.
Much attention has been paid to the disproportionate rates of SARS‐CoV‐2 infection in Hispanic and black non‐Hispanic populations in the United States.4, 5 The reasons for this relationship are not fully understood. Theories include increased exposure to the virus among Hispanic and black non‐Hispanic populations owing to employment, economic hardship, dense living conditions, and other general disparities.4, 5 Here, we demonstrated additional racial/ethnic influences on relationship between ABO group/Rh type and SARS‐CoV‐2 positivity.
One explanation for variations among studies is differences in the underlying distributions of blood groups/types by race/ethnicity in the populations studied. The race/ethnicity distribution for the subset of females with available data in this study was remarkably similar to estimates for the total U.S. population.6 ABO blood types are known to influence susceptibility to other infectious agents, including the severe acute respiratory syndrome‐associated coronavirus‐1 (SARS‐CoV‐1), where similar associations with blood group have been described.1, 2 The ABO antigens are carbohydrate‐enriched epitopes present on erythrocytes, endothelial cells, and other specialized tissues and secreted within certain body fluids of some individuals. These antigens induce a potent immune response, triggering isoagglutinin antibodies against non‐expressed ABO antigens. The spike proteins of SARS viruses also express carbohydrate‐rich moieties, as well as ABO antigens borrowed from the infected host. In this way, type O individuals, whose blood naturally contains both anti‐A and anti‐B isoagglutinin antibodies, are thought to have an inherent immune advantage against SARS viral infections.1, 2
The Rh blood type consists of more than 50 protein antigens, the most clinically relevant of which are D, C, c, E, and e. The RH locus encodes two genes RHD and RHCE. An individual’s Rh type is largely determined by the presence or absence of the D antigen on erythrocytes, Rh+ or Rh‐, respectively. The Rh antigens complex with associated glycoproteins on the red blood cell surface, but physiologic roles of RhD and RhE have yet to be elucidated. The association between Rh + blood and SARS‐CoV‐2 positivity merits further investigation.
This study was limited by several factors. The majority of those studied were likely pregnant at the time of ABO/Rh testing, but not necessarily pregnant at the time of SARS‐CoV‐2 testing. It is unclear how pregnancy and its associated immunotolerance affect SARS‐CoV‐2 positivity rates. People with symptoms, or high exposure risk, for example, healthcare workers, are theoretically more likely to be tested for SARS‐CoV‐2. In addition, race/ethnicity data were reported by the ordering clinician and were only available for 32.2% of the study cohort. However, the group of females with race/ethnicity available (n = 88 975) still represents one of the largest known studies to date comparing the association between ABO/Rh and SARS‐CoV‐2 positivity. No clinical information was available to corroborate test results, correlate outcome, or assess clinical course.
In summary, an association between ABO/Rh and SARS‐CoV‐2 positivity was confirmed but greatly attenuated after factoring in race/ethnicity. Future studies to evaluate the influence of race/ethnicity on COVID‐19 risk and clinical course are necessary for comprehensive assessment of the impact of blood group/Rh type on infection and disease.
Association of ABO/Rh with SARS‐CoV‐2 positivity: The role of race and ethnicity in a female cohort
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“Results from SARS‐CoV‐2 RNA nucleic acid amplification tests (NAAT) performed March through July 2020 were matched with ABO/Rh test results obtained for the same individual since January 2010. Only one SARS‐CoV‐2 result per patient was considered; a patient was considered to have a positive result if any SARS‐CoV‐2 test result was positive. The ABO/Rh testing is generally performed as part of maternal screening; males were excluded. The influence of race/ethnicity on the associations of ABO type/Rh group with SARS CoV‐2 positivity was assessed in a subset of females with available race/ethnicity data.”
“The study cohort comprised 276,536 females with matched SARS-CoV-2 and ABO-Rh results from all 50 American states and the District of Columbia. There were 34,178 females who were SARS-CoV-2 positive (12.4%, 95% CI 12.2%-12.5%). The median patient age at the time of SARS-CoV-2 testing was 34.4 (IQR 29.2-40.0) years,”
“The SARS‐CoV‐2 positivity rate was 38% higher in Rh+ patients (12.7%, 95% CI 12.6%‐12.8%) than in Rh‐ patients (9.2%, 95% CI 8.9%‐9.5%) (P < .001). " … 12.7% vs 9.2%
"However, after adjusting for race/ethnicity, the relationship between type O and SARS‐CoV‐2 reversed from predictive to protective. Type O and Rh + blood is more prevalent in Hispanics and black non‐Hispanics, two groups in our study with the highest proportions of positive SARS‐CoV‐2 tests. Thus we conclude, in concordance with findings from other studies,1 that type O blood is slightly protective against SARS‐CoV‐2 positivity once race/ethnicity has been considered. The multivariable model also demonstrated that the influence of Rh+ blood type was attenuated when adjusted for race/ethnicity, suggesting that the association between ABO/Rh and SARS‐CoV‐2 positivity is strongly influenced by race/ethnicity."
"White non‐Hispanic females were more than twice as likely to be Rh‐ (15.1%) compared to other groups, including “other” race/ethnicity (6.6%), Hispanic (6.4%), and black non‐Hispanic (6.1%) groups (P < .001 for all comparisons). Hispanic females had the highest SARS‐CoV‐2 positivity rate (21.4%, 95% CI 20.9%‐21.9%), followed by black non‐Hispanic (16.3%, 95% CI 15.7%‐16.9%), “other” race/ethnicity (12.8%, 95% CI 12.3%‐13.4%), and white non‐Hispanic (7.2%, 95% CI 6.9%‐7.4%) females."
of those classified as White non‐Hispanic females: 15.1% were RhD- and so 84.9% had to be RhD+ … which is essentially the #'s i use for the population percentages of this group in the USA.
all the other women classified as RhD- were in the 6.1-6.6% range which seems about right imo for the USA. still all the other White non-Hispanic women had much higher positivity rates: 7.2% vs 12.8%, 16.3%, & 21.4%. population density appears to be a very important factor in CVD19 infection rates. that may explain some of the differences.
i wonder if the RhoGAM shot affects the results? also they were just testing for the virus & not commenting on the outcomes and/or the severity of those women infected? being RhD- is once again helpful & seems even more helpful than being just type O.
when will they ever consider/look at those w/ the CCR5-delta32 mutation? i still believe this mutation – that is largely a European/Scandinavian people & and their descendants trait – is making a noticeable difference, especially if white blood cells are affected by CVD19 – which certainly seems to be the case. perhaps it's because testing for this is too expensive. regardless – they can still test the deceased i would think. – just looking for the truth here, i am –
Have you looked into IFNAR2 before?
i’ve seen studies mentioning interferon before regarding CVD19, but i took quick look now and found the following:
Interferon https://en.wikipedia.org/wiki/Interferon
“”Interferons (IFNs, /ˌɪntərˈfɪərɒn/[1]) are a group of signaling proteins[2] made and released by host cells in response to the presence of several viruses. In a typical scenario, a virus-infected cell will release interferons causing nearby cells to heighten their anti-viral defenses.
IFNs belong to the large class of proteins known as cytokines, molecules used for communication between cells to trigger the protective defenses of the immune system that help eradicate pathogens.[3] Interferons are named for their ability to “interfere” with viral replication[3] by protecting cells from virus infections. IFNs also have various other functions: they activate immune cells, such as natural killer cells and macrophages; …””
IFNAR2 https://en.wikipedia.org/wiki/IFNAR2
“Interferon-alpha/beta receptor beta chain is a protein that in humans is encoded by the IFNAR2 gene.”
IFNAR2 – interferon (alpha, beta and omega) receptor 2
https://www.wikigenes.org/e/gene/e/3455.html
Found: genes that sway the course of the coronavirus
By Jocelyn KaiserOct. 13, 2020 , 1:25 PM
https://www.sciencemag.org/news/2020/10/found-genes-sway-course-coronavirus
“”In June, one such genomewide association study in The New England Journal of Medicine (NEJM) found two “hits” linked to respiratory failure in 1600 Italian and Spanish COVID-19 patients: a marker within the ABO gene, which determines a person’s blood type, and a stretch of chromosome 3 that holds a half-dozen genes.””
“”The new study confirmed the chromosome 3 region’s involvement. And because 74% of its patients were so sick that they needed invasive ventilation, it had the statistical strength to reveal other markers, elsewhere in the genome, linked to severe COVID-19. One find is a gene called IFNAR2 that codes for a cell receptor for interferon, a powerful molecular messenger that rallies the immune defenses when a virus invades a cell. A variant of IFNAR2 found in one in four Europeans raised the risk of severe COVID-19 by 30%. Baillie says the IFNAR2 hit is “entirely complementary” to a finding reported in Science last month: very rare mutations that disable IFNAR2 and seven other interferon genes may explain about 4% of severe
COVID-19 cases.””
“”The chromosome 3 region still stands out as the most powerful genetic actor: A single copy of the disease-associated variant more than doubles an infected person’s odds of developing severe COVID-19. Evolutionary biologists reported last month in Nature that this suspicious region actually came from Neanderthals, through interbreeding with our species tens of thousands of years ago. It is now found in about 16% of Europeans and 50% of South Asians.””
“”But the specific chromosome 3 gene or genes at play remain elusive. By analyzing gene activity data from normal lung tissue of people with and without the variant, the U.K. team homed in on CCR2, a gene that encodes a receptor for cytokine proteins that play a role in inflammation. But other data discussed at last week’s meeting point to SLC6Z20, which codes for a protein that interacts with the main cell receptor used by SARS-CoV-2 to enter cells. “I don’t think anyone at this point has a clear understanding of what are the underlying genes” for the chromosome 3 link, says Andrea Ganna of the University of Helsinki, who co-leads the COVID-19 Host Genetics Initiative.””
“”Geneticists have had little luck so far identifying gene variants that explain why COVID-19 has hit Black people in the United States and United Kingdom particularly hard. The chromosome 3 variant is absent in most people of African ancestry.””
“”A variant of IFNAR2 found in one in four Europeans raised the risk of severe COVID-19 by 30%. Baillie says the IFNAR2 hit is “entirely complementary” to a finding reported in Science last month: very rare mutations that disable IFNAR2 and seven other interferon genes may explain about 4% of severe COVID-19 cases.””
“It is now found in about 16% of Europeans and 50% of South Asians.””
“The chromosome 3 variant is absent in most people of African ancestry.”
seems like this IFNAR2 variant makes things worse…and folks w/ strong African ancestry don’t have IFNAR2 because they didn’t mix w/ Neanderthals. so, something else like CCR5-delta32 could be making at least some of the difference (or it could be helping to off-set this IFNAR2 CVD19 severity enhancing problem) for Europeans & Scandinavians (and their descendants and those people in neighboring areas) w/ those who may have the complete mutation or just 1/2 of it.
clarifying: variants and mutations of IFNAR2 seems to be the problem/make CVD19 worse. Africans likely have IFNAR2, but not the variants & mutations; if, i understand the article i quoted above properly.
Thank you, Ken. I have been receiving several suggestions and questions from people and will look more into the following:
1) Are people with blood type O negative less likely to carry IFNAR2?
2) Does absence of IFNAR2 impact likelihood of fatality and how?
3) Non-secretors have reduced susceptibility to the most common strains of norovirus. How about other viruses?
These are the top ones for me right now to shine more light into what we might have been missing.
i think everyone carries IFNAR2 now…as i just added above/clarifying: variants/mutations of IFNAR2 seem to be the problem.
Secretor polymorphism and human immunodeficiency virus infection in Senegalese women
https://pubmed.ncbi.nlm.nih.gov/10669366/
The FUT2 gene encodes the enzyme alpha (1,2) fucosyltransferase, which determines expression of blood-group antigens on mucosal epithelial cell surfaces and in secretions. Homozygotes for a specific stop mutation in FUT2 (nonsecretors) cannot produce this enzyme and thus are unable to express blood group antigens. Nonsecretor status is associated with a decreased risk of several respiratory viral infections. By use of molecular genotyping, 2 populations of Senegalese women were examined for polymorphisms of the FUT2 gene. Among Senegalese commercial sex workers, absence of FUT2 (nonsecretor genotype) was associated with reduced risk of human immunodeficiency virus (HIV) type 1 infection (odds ratio [OR] adjusted for cervical and vaginal infection, 0.18; 95% confidence interval [CI], 0.04-0.90) and HIV-2 infection (adjusted OR, 0.43; 95% CI, 0.13-1.39), although the latter was not statistically significant. Modification of cell surface carbohydrates at mucosal surfaces determined by the FUT2 gene may underlie the protective association against heterosexual HIV infection.
Well Done (Twice), Mike Dammann !!! That’s The Key!!!
Apologies for my delayed Greetings, Dear Friend : Recovering From a Domestic Accident That Was Sufficiently Painful To End In Clinical ER and Hospitalization… Your Excellent “Letter” (Resumes Your Beautiful Research) is a matter of Complementary Analysis For That One of 23andme on Race and COVID-19! Very Proud and Honored to Be Your Peruvian Friend, Really!
As A Fact, I’m Trying to Get Contact With Mrs Mazzetti Soler (Our Minister of Health) and, As You Know, She Decided to Walk Aside Because The Political Situation (Strike In Peru: Congress Vs President Vizcarra–> Strike for 6 Days–> Incredibly, Population From All Citizens From Peruvian Regions (Without Any Doubt or Fear from COVID-19) Protests–> 2 Young Persons Died (One of them, Student From The University I’m Teaching) –> Rendition of the Imposed President and Elected Transition Guys… A Soup of Different Emotional Elements That You May Be Aware (Informated by International Press, Maybe)… Fffiu !!!
Even Though, I’m sure that you’ll Understand My Affection for This Country as Well: Mrs Mazzetti Soler Returned to Ministry of Health a Week Ago and is now a possibility for The Research Objective With Two or 3 Published Research Work, including Your’s.
If you Want to Review the numbers That Richard Youatt for Rh Factor Negatives in Peru Are Quite Accurate and True: We Have Had to Lockdown All The Country to Save Lives… or I’m Wrong, Viewing what Happened in Mexico and USA?…
So Much Pain For All The People that have Died Because their Exposure and Secondary Illnesses (Here we have too Much Diabetics, Overweight and Hypertension).
In The Other Hand, There’s 2 Ideas That I’ve Traduced from my Intuition More Than anything we can call A Real “scientific Intellectual Reasoning” :
1) If We Come From Genetic Ancestors and Having Negative Blood but we are Rhesus Positive … Can we be Carriers/Spreaders of COVID-19 Without Doing Symptoms, More if we are Secretor Type?
2) Are There any form to Probe It (The Fact of being Secretor Spreader)? Maybe Only By PCR Positive Test With Nasal Oropharyngeal Measures? And If It’s Positive, See a manner to consider a Laboratory Specialized in Genetics (IDK, 23andme) That can Help Us To Probe The Ancestry of The Candidates?
Raw Ideas and Fulfilled of impressions More Than Facts…
A Pleasure to contact One more time with you, Dear Friend(s).
Here’s 07:10 PM and Hope You’re All Well and Thank You Very Much!
Buenas Noches
Jorge
Well Done (Twice), Mike Dammann !!! That’s The Key!!!
Apologies for my delayed Greetings, Dear Friend : Recovering From a Domestic Accident That Was Sufficiently Painful To End In Clinical ER and Hospitalization… Your Excellent “Letter” (Resumes Your Beautiful Research) is a matter of Complementary Analysis For That One of 23andme on Race and COVID-19! Very Proud and Honored to Be Your Peruvian Friend, Really!
As A Fact, I’m Trying to Get Contact With Mrs Mazzetti Soler (Our Minister of Health) and, As You Know, She Decided to Walk Aside Because The Political Situation (Strike In Peru: Congress Vs President Vizcarra–> Strike for 6 Days–> Incredibly, Population From All Citizens From Peruvian Regions (Without Any Doubt or Fear from COVID-19) Protests–> 2 Young Persons Died (One of them, Student From The University I’m Teaching) –> Rendition of the Imposed President and Elected Transition Guys… A Soup of Different Emotional Elements That You May Be Aware (Informated by International Press, Maybe)… Fffiu !!!
Even Though, I’m sure that you’ll Understand My Affection for This Country as Well: Mrs Mazzetti Soler Returned to Ministry of Health a Week Ago and is now a possibility for The Research Objective With Two or 3 Published Research Work, including Your’s.
If you Want to Review the numbers That Richard Youatt for Rh Factor Negatives in Peru Are Quite Accurate and True: We Have Had to Lockdown All The Country to Save Lives… or I’m Wrong, Viewing what Happened in Mexico and USA?…
So Much Pain For All The People that have Died Because their Exposure and Secondary Illnesses (Here we have too Much Diabetics, Overweight and Hypertension).
In The Other Hand, There’s 2 Ideas That I’ve Traduced from my Intuition More Than anything we can call A Real “scientific Intellectual Reasoning” :
1) If We Come From Genetic Ancestors and Having Negative Blood but we are Rhesus Positive … Can we be Carriers/Spreaders of COVID-19 Without Doing Symptoms, More if we are Secretor Type?
2) Are There any form to Probe It (The Fact of being Secretor Spreader)? Maybe Only By PCR Positive Test With Nasal Oropharyngeal Measures? And If It’s Positive, See a manner to consider a Laboratory Specialized in Genetics (IDK, 23andme) That can Help Us To Probe The Ancestry of The Candidates?
Raw Ideas and Fulfilled of impressions More Than Facts…
A Pleasure to contact One more time with you, Dear Friend(s).
Here’s 04:30 PM and Hope You’re All Well and Thank You Very Much for Being as You Are. Maybe I’ll Try to training in my every Time Dedication to Studying A post Master or Degree in my Always beloved Molecular Genetics! (As Dr. Timothy Crow, From England, Suggests Me in the late 1985)… Why not now?
Buenas Noches
Jorge
It seems they’ve identified the genes for increased protection from covid. Without one of these, you have more viral resistance.
https://www.cnbc.com/2020/11/20/crispr-scientists-claim-identified-genes-that-protect-against-covid.html