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Thread: SARS-CoV-2 respiratory failure: risk SNPs, Bloodtype A is a risk, O is protective

  1. #81
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    Synairgen said a drug — SNG001 — was used as a treatment in a new trial.
    The drug showed a 79% lower risk of patients developing severe disease compared to a placebo used in the trial.
    The drug “is a formulation of a naturally occurring antiviral protein called interferon beta and is inhaled directly into the lungs in the hope of stimulating an immune response,” according to CNBC.
    https://www.deseret.com/u-s-world/20...through-sng001

  2. #82
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    Molecular Underpinnings of Severe Coronavirus Disease 2019

    Molecular Underpinnings of Severe Coronavirus Disease 2019
    Robert M. Plenge, MD, PhD
    The molecular underpinnings of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the disease it causes, coronavirus disease 2019 (COVID-19), are poorly understood. Inherited genetic variation is an important tool to disentangle cause and consequence, which in turn can generate insights to guide therapeutic interventions to prevent or treat disease. To date, little is known about genetic susceptibility to SARS-CoV-2 infection and severe forms of COVID-19.1,2

    In this issue of JAMA, van der Made and colleagues3 describe 2 independent families with rare germline variants in an innate immune-sensing gene, toll-like receptor 7 (TLR7), that lead to severe disease in males who inherit the mutated gene on a single copy of their X chromosome. The study implicates TLR7 as a critical node in recognizing SARS-CoV-2 and initiating an early immune response to clear the virus and prevent the development of COVID-19.
    YFull: YF14620 (Dante Labs 2018)

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  4. #83
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    Longitudinal analyses reveal immunological misfiring in severe COVID-19

    Longitudinal analyses reveal immunological misfiring in severe COVID-19
    Carolina Lucas, Patrick Wong, Jon Klein, Tiago B. R. Castro, Julio Silva, Maria Sundaram, Mallory K. Ellingson, Tianyang Mao, Ji Eun Oh, Benjamin Israelow, Takehiro Takahashi, Maria Tokuyama, Peiwen Lu, Arvind Venkataraman, Annsea Park, Subhasis Mohanty, Haowei Wang, Anne L. Wyllie, Chantal B. F. Vogels, Rebecca Earnest, Sarah Lapidus, Isabel M. Ott, Adam J. Moore, M. Catherine Muenker, John B. Fournier, Melissa Campbell, Camila D. Odio, Arnau Casanovas-Massana, Yale IMPACT Team, Roy Herbst, Albert C. Shaw, Ruslan Medzhitov, Wade L. Schulz, Nathan D. Grubaugh, Charles Dela Cruz, Shelli Farhadian, Albert I. Ko, Saad B. Omer & Akiko Iwasaki

    Abstract
    Recent studies have provided insights into the pathogenesis of coronavirus disease 2019 (COVID-19)1–4. Yet, longitudinal immunological correlates of disease outcome remain unclear. Here, we serially analysed immune responses in 113 COVID-19 patients with moderate (non-ICU) and severe (ICU) disease. Immune profiling revealed an overall increase in innate cell lineages with a concomitant reduction in T cell number. We identify an association between early, elevated cytokines and worse disease outcomes. Following an early increase in cytokines, COVID-19 patients with moderate disease displayed a progressive reduction in type-1 (antiviral) and type-3 (antifungal) responses. In contrast, patients with severe disease maintained these elevated responses throughout the course of disease. Moreover, severe disease was accompanied by an increase in multiple type 2 (anti-helminths) effectors including, IL-5, IL-13, IgE and eosinophils. Unsupervised clustering analysis identified 4 immune signatures, representing (A) growth factors, ( type-2/3 cytokines, (C) mixed type-1/2/3 cytokines, and (D) chemokines that correlated with three distinct disease trajectories of patients. The immune profile of patients who recovered with moderate disease was enriched in tissue reparative growth factor signature (A), while the profile for those with worsened disease trajectory had elevated levels of all four signatures. Thus, we identified development of a maladapted immune response profile associated with severe COVID-19 outcome and early immune signatures that correlate with divergent disease trajectories
    YFull: YF14620 (Dante Labs 2018)

  5. #84
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    Longitudinal analyses reveal immunological misfiring in severe COVID-19

    Longitudinal analyses reveal immunological misfiring in severe COVID-19
    Carolina Lucas, Patrick Wong, Jon Klein, Tiago B. R. Castro, Julio Silva, Maria Sundaram, Mallory K. Ellingson, Tianyang Mao, Ji Eun Oh, Benjamin Israelow, Takehiro Takahashi, Maria Tokuyama, Peiwen Lu, Arvind Venkataraman, Annsea Park, Subhasis Mohanty, Haowei Wang, Anne L. Wyllie, Chantal B. F. Vogels, Rebecca Earnest, Sarah Lapidus, Isabel M. Ott, Adam J. Moore, M. Catherine Muenker, John B. Fournier, Melissa Campbell, Camila D. Odio, Arnau Casanovas-Massana, Yale IMPACT Team, Roy Herbst, Albert C. Shaw, Ruslan Medzhitov, Wade L. Schulz, Nathan D. Grubaugh, Charles Dela Cruz, Shelli Farhadian, Albert I. Ko, Saad B. Omer & Akiko Iwasaki

    Abstract
    Recent studies have provided insights into the pathogenesis of coronavirus disease 2019 (COVID-19)1–4. Yet, longitudinal immunological correlates of disease outcome remain unclear. Here, we serially analysed immune responses in 113 COVID-19 patients with moderate (non-ICU) and severe (ICU) disease. Immune profiling revealed an overall increase in innate cell lineages with a concomitant reduction in T cell number. We identify an association between early, elevated cytokines and worse disease outcomes. Following an early increase in cytokines, COVID-19 patients with moderate disease displayed a progressive reduction in type-1 (antiviral) and type-3 (antifungal) responses. In contrast, patients with severe disease maintained these elevated responses throughout the course of disease. Moreover, severe disease was accompanied by an increase in multiple type 2 (anti-helminths) effectors including, IL-5, IL-13, IgE and eosinophils. Unsupervised clustering analysis identified 4 immune signatures, representing (A) growth factors, (B ) type-2/3 cytokines, (C) mixed type-1/2/3 cytokines, and (D) chemokines that correlated with three distinct disease trajectories of patients. The immune profile of patients who recovered with moderate disease was enriched in tissue reparative growth factor signature (A), while the profile for those with worsened disease trajectory had elevated levels of all four signatures. Thus, we identified development of a maladapted immune response profile associated with severe COVID-19 outcome and early immune signatures that correlate with divergent disease trajectories
    YFull: YF14620 (Dante Labs 2018)

  6. #85
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    A+ here and I got the GT variant. No one in my family as far as I know has caught it.

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  8. #86
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    https://www.smh.com.au/national/scie...18-p55mw2.html

    Evidence is emerging worldwide showing between 20 and 50 per cent of people who have never been exposed to COVID-19 have immune cells that can recognise and react to the virus.

    The discovery of T cell cross-reactivity has excited immunologists, who hope it could explain some of the mysteries that surround the virus, such as why some people get so much sicker than others.


    My Path = ( K-M9+, TL-P326+, T-M184+, L490+, M70+, PF5664+, L131+, L446+, CTS933+, CTS3767+, CTS8862+, Z19945+, BY143483 )


    Grandfather via paternal grandmother = I1-L22 ydna
    Great grandmother paternal side = T1a1e mtdna

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    According to a study by David Ellinghaus et al. published in NEJM https://www.nejm.org/doi/full/10.1056/NEJMoa2020283 an indicator for a major risk for respiratory failure susceptibility is located in an intronic region on Chromosome 3 and is designated as rs11385942.

    See also here on SNPedia: https://www.snpedia.com/index.php/Rs11385942

    SNP rs11385942 was found 77% more frequently in Covid-19 patients than in the control group.

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    Quote Originally Posted by Frank&Frei View Post
    According to a study by David Ellinghaus et al. published in NEJM https://www.nejm.org/doi/full/10.1056/NEJMoa2020283 an indicator for a major risk for respiratory failure susceptibility is located in an intronic region on Chromosome 3 and is designated as rs11385942.

    See also here on SNPedia: https://www.snpedia.com/index.php/Rs11385942

    SNP rs11385942 was found 77% more frequently in Covid-19 patients than in the control group.
    Hooray!

    I don't have it!

    My rs10490770 comes up as (T;T) which is the "good" allele.
    Last edited by dosas; 08-21-2020 at 01:16 PM.
    53.52% Greek_Central_Macedonia + 46.48% Greek_Trabzon @ 0.018

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  14. #89
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    Quote Originally Posted by dosas View Post
    Hooray!

    I don't have it!

    My rs10490770 comes up as (T;T) which is the "good" allele.
    Good for you dosas.

    I recently ordered a test for SNP rs11385942 from a well-known and reputable lab. The processing of the sample is done by Sanger Sequencing; it will take a while to see the result. The price for the test is 18 $ so it is affordable.
    Last edited by Frank&Frei; 08-23-2020 at 07:39 AM.

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    Some additional interesting information regarding SNP rs11385942 is available here : https://www.biorxiv.org/content/10.1....186296v1.full

    Paleoanthropologists Hugo Zeberg and Svante Pääbo state that this particular risk insertion variant is inherited by the Neandertals.

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