STUDY: Ashkenazi Jews and Amish Are Least Susceptible to Covid-19 | Aharon Bendavid

During my research regarding Covid-19, I came across this study. While I found the information compelling, I honestly did not know how to write an article about it, given the amount of data it sourced. Rather than give up, I decided to simply write one of the major conclusions in the title of this piece. I will repeat it here:

Ashkenazi Jews and Amish Are Least Susceptible to Covid-19

The study is entitled:

New Insights into Genetic Susceptibility Of COVID-19: An ACE2 And TMPRSS2 Polymorphism Analysis published by BMC Medicine.

Hou, Y., Zhao, J., Martin, W. et al. new insights into genetic susceptibility of COVID-19: an ACE2 and TMPRSS2 polymorphism analysis. BMC Med 18, 216 (2020).

I do not claim to have any medical knowledge. I am not a doctor, epidemiologist, nor a researcher. The key takeaway for me is that the immune receptor called ACE2 is not susceptible to any disruption by the Covid-19 virus in Ashkenazi Jews.

Anti-Semites have used parts of this study to develop a conspiracy theory where they are convinced that Covid-19 is a plot by Jews to dominate the world. Anti-Semites have used this canard for almost everything under the sun, from Jews controlling banking, Wall Street and the so-called “entertainment industry” (Motion pictures and recording), for just a few examples.

The following are unedited excerpts from the actual study and all the sources for those who may be capable of understanding them. Again, the bottom line is: the immune receptor called ACE2 is not susceptible to any disruption by the Covid-19 virus in Ashkenazi Jews.

You can draw your own conclusions, as for me, it means that cases of Covid-19 would be mild, not lasting long, and would develop natural immunity and thus herd immunity across the Ashkenazi population. You can see the graphic results of the study below in Fig. 1b.

ACE2 polymorphism analysis across different populations. Here, we investigated genetic susceptibility to COVID19 by examining DNA polymorphisms in ACE2 (OMIM 300335) and TMPRSS2 (OMIM 602060) genes. We assembled a total of 437 non-synonymous singlenucleotide variants (SNVs) in the protein-coding regions of ACE2 and TMPRSS2 (Fig. 1a) from three databases: (i) Genome Aggregation Database (gnomAD v3:, covering 9 geographical areas), (ii) Exome Sequencing Project (ESP: edu/EVS/), and (iii) 1000 Genomes Project (1KGP, www. We used ANNOVAR [9] to annotate all non-synonymous variants. By applying Polyphen2 and CADD (Combined Annotation Dependent Depletion) scores, we identified 63 potentially deleterious variants in ACE2 (61 in gnomAD) and 68 deleterious variants in TMPRSS2 (63 in gnomAD). We found that the distribution of deleterious variants in ACE2 differs among 9 populations in gnomAD (v3). Specifically, 39% (24/61) and 54% (33/61) of deleterious variants in ACE2 occur in African/African-American (AFR) and Non-Finnish European (EUR) populations, respectively (Fig. 1b). Prevalence of deleterious variants among Latino/Admixed American (AMR), East Asian (EAS), Finnish (FIN), and South Asian (SAS) populations is 2–10%, while Amish (AMI) and

Ashkenazi Jewish (ASJ) populations do not appear to carry such variants in ACE2 coding regions

 Fig. 1: The coding-region variants in ACE2 and TMPRSS2 from ~ 81,000 human genomes across 8 populations. a Coding-region variants in the genes encoding angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) across three human genome databases: (i) Genome Aggregation Database (gnomAD v3), (ii) Exome Sequencing Project (ESP), and (iii) 1000 Genomes Project (1KGP). SARS-CoV-2 utilizes the host cell factors angiotensin-converting enzyme 2 (ACE2) for entry into cells and the host transmembrane serine protease TMPRSS2 for SARS-CoV-2 spike (S) protein priming, offering potential pathway for therapeutic development in treatment of COVID-19. b Distribution of 61 deleterious variants in the ACE2 coding region identified in gnomAD (v3). Polyphen2 > 0.96 and CADD scores > 20 as cutoff identify putative deleterious variants. The upper panel using 3 colors shows the functional domains of ACE2, and the height of the vertical line represents the number of populations that carry this variant. The lower heatmap shows the allele frequencies (color key) of a variant across different populations. c Distributions of 63 putative deleterious variants in the TMPRSS2 coding region using the same approach of b. AFR, African/African-American; AMI, Amish; AMR, Latino/Admixed American; ASJ, Ashkenazi Jewish; EAS, East Asian; FIN, Finnish; EUR, Non-Finnish European; SAS, South Asian; PNA, population not assigned.


This comprehensive comparative genetic analysis of approximately 81,000 human genomes suggested possible associations of ACE2 and TMPRSS2 DNA polymorphisms with COVID-19 susceptibility, severity, and clinical outcomes. We found that ACE2 polymorphisms were more likely to be associated with cardiovascular and pulmonary conditions by altering the angiotensinogen-ACE2 interactions, such as p.Arg514Gly in the African/African-American population. Unique but prevalent polymorphisms in TMPRSS2, including p.Val160Met (rs12329760), may provide potential explanations for differential genetic susceptibility to COVID19 as well as for risk factors, including cancer and the high-risk group of male patients. We highlighted that polymorphisms in ACE2 or TMPRSS2 could guide personalized treatments (i.e., hydroxychloroquine and camostat) for COVID-19. In summary, this study suggested that ACE2 or TMPRSS2 DNA polymorphisms were likely associated with genetic susceptibility to COVID-19, which calls for a human genetics initiative for fighting the COVID-19 pandemic.

Availability of data and materials All population genetic data used in this study are free and available at three databases: (i) Genome Aggregation Database (gnomAD v3: gnomad., covering 9 geographical areas), (ii) Exome Sequencing Project (ESP:, and (iii) 1000 Genomes Project (1KGP,

Yuan Hou1, Junfei Zhao2, William Martin1, Asha Kallianpur1,3, Mina K. Chung3,4,5, Lara Jehi5, Nima Sharifi3,5, Serpil Erzurum3,5, Charis Eng1,3,6,7 and Feixiong Cheng1,3,7*

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This work was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health (NIH) under Award Number R00HL138272 and the National Institute of Aging under Award Number R01AG066707 to F.C. This work was supported, in part, by the VeloSano Pilot Program (Cleveland Clinic Taussig Cancer Institute).

Author information


  1. Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA

Yuan Hou, William Martin, Asha Kallianpur, Charis Eng & Feixiong Cheng

  1. Department of Systems Biology and Department of Biomedical Informatics, Herbert Irving Comprehensive Center, Columbia University, New York, NY, 10032, USA

Junfei Zhao

  1. Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, 44195, USA

Asha Kallianpur, Mina K. Chung, Nima Sharifi, Serpil Erzurum, Charis Eng & Feixiong Cheng

  1. Department of Cardiovascular Medicine, Heart, Vascular and Thoracic Institute, Cleveland Clinic, Cleveland, OH, 44195, USA

Mina K. Chung

  1. Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA

Mina K. Chung, Lara Jehi, Nima Sharifi & Serpil Erzurum

  1. Department of Genetics and Genome Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH, 44106, USA

Charis Eng

  1. Case Comprehensive Cancer Center, School of Medicine, Case Western Reserve University, Cleveland, OH, 44106, USA

Charis Eng & Feixiong Cheng

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  1. disclaimer: I did not read through this article, because I don’t understand the scientific terms. I am not disqualifying this, just adding my own opinion of why Jews and Amish likely have the lower cases of covid. This is because these 2 groups are least likely to test for covid when sick, so there are less documented cases – emphasize documented

  2. As a medical doctor who drove through Amish country during the height of the pandemic, I can tell you that our resistance comes not from mutations to the ACE receptor, but due to the fact that the Amish and the Frum communities are the youngest demographic in the country, and also because both communities ignored the quarantine and masking mandates (the Amish more so than us), so were already exposed.

    • I can’t even count the number of sources in this article. Are you amongst them? Your sourcing a drive through Amish country? You have to be kidding. You are Dr. Moshe who? Sorry doc, your opinion is NOT “due to the [your] fact”. If you are truly a doctor, kindly post your practice name so I can avoid it at all costs.

  3. Anyone have a count of how many ashkenazi funerals we had??????????? Not to mention the amount if people that were deathly sick ????
    Just here in Lakewood we are now in the period of yahrzeits almost daily from civic deaths

  4. The reason, by and large that the frum community and the Amish have had a greater success with skirting Covid is because they both don’t have televisions. (and we also have a very healthy dose of skepticism)

    Fear drives illness.

  5. I did some research. Not all Yidden who go by Ashkenazi are truly genetically so. A DNA test can show genetic discrepancies. Mine shows somewhere we have Sephardi mutations. That makes sense because my great grandparents named Epstein were descendants of the Torah Temimah who was Sephardic.

  6. Seems a bit too coincidental to my liking that the 2 most insular communities are the the most resistant. While certainly the virus, because is manmade can certainly have been engineered to target certain demographics… and anecdotal evidence does in fact support this as certain communities as the asian/black/latin were hit harder than Caucasians. But considering that ashkenazi jews and the amish are of very different backgrounds, it doesn’t seem probable. But then again… it’s not the first thing the chinese botched up on programming correctly… they aren’t great at their own creations.. they do much better when stealing American designs and copying them.

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