A prenylated dsRNA sensor protects against severe COVID-19

I was recently accused of making claims here without any evidence. I believe it was in response to my assertion that most severe cases of C19 are likely due to genetic factors. Each week, I read dozens of papers, and my ATS posts are frequently based on a cumulative body of knowledge for which there is often no single link. I looked through previous studies I have read and came across this one from September, which indicated a strong link between a genetic component and severe C19. This is just one of many papers on genetic factors for severe C19 that I've read. I often assume that what I say is common knowledge for anyone who puts even a minimal effort into keeping current with all of the relative research or trends.

According to research, a component of the human interferon system that stimulates SARS2 cellular defenses appears to be faulty in a subset of individuals. In hospitalized individuals with this immune system impairment, C19 results were more severe. The findings indicate that interferon defense is an important part of a protective antiviral response. C19 illness is heterogeneous, making it difficult to anticipate how an infection would progress in an individual. Interferons are the first signals for cellular defenses after a viral infection. Knowing that interferon signaling deficiencies are linked to more severe C19, Arthur Wickenhagen et al. employed interferon-stimulated gene expression screening on human lung cells to find a gene for an enzyme, OAS1, that reacts to interferon signals, causing the enzyme to fight viral infection.

SARS2 replication has been demonstrated to be inhibited by OAS1. OAS1 is linked to membranes via a prenyl group in most animals. However, billions of people lack the prenylated OAS1 haplotype, including many people who suffer with severe C19. Wickenhagen investigated if the non-prenylated OAS1 haplotype has the same anti-SARS2 activity as the prenylated counterpart. "Remarkably, the non-prenylated version had no discernible anti-SARS-CoV-2 action," they wrote. They found that the absence of prenylated OAS1 was related with more severe disease after evaluating the transcriptomes of approximately 500 C19 individuals with varying disease outcomes. The discovery that prenylation is required for antiviral action motivated the researchers to investigate this element of OAS1 biology in animals other than humans. There is a lot of interest right now in figuring out what biological features bats have that predispose them to being viral reservoirs. Horseshoe bats do not have the prenylated OAS1 haplotype, according to Wickenhagen & colleagues. According to them, this could explain why horseshoe bats are particularly prolific sarbecovirus reservoir hosts.

A prenylated dsRNA sensor protects against severe COVID-19

read about this a couple of days ago and checked for susceptability on livewello, which is a gene app I use. Someone did create the template, but the data on the five risk snps including this one was not gathered by the Ancestry site. I don't know if other ancestry sites collect this snp or not. Maybe I should get a full genome done some day.

a reply to: rickymouse

Are you sure that Ancestry didn't genotype rs10774671 for you? I just checked and they did for mine. I've used livewello, but like promethease.com better.

Something is going on with a group of people that regardless of having covid, getting the jab and boosters do not show any type of antibodies.

My husband knows one that had covid, recuperated, still got the jab due to his government job, then tested positive for covid but did not got sick second time, soo he decided to get the antibodies test, came back negative, he went back and was given a booster still no antibodies, then he got an antibody infusion, was tested again and negative for antibodies, now his doctor wants him to do an entire panel for blood disorders and immune problems.

Still he is healthy and have not problems.

My daughter have a friend that is traveling oversea for the Christmas, got the two jabs tested positive for covid, wanted to get her antibodies check, because she wants to be negative for travelling, well no antibodies, her doctor recommended the boosters, again positive for covid as expected after the jab but no antibodies, her doctor went ahead and gave her another booster shot, again no antibodies.

She has no symptoms and otherwise healthy, will be getting also more test to see what is going on.

Now has anybody hear about this type of condition? after been jabbed?

a reply to: marg6043

I'm one of those who didn't produce any detectable antibodies despite testing positive. My assumption was that I didn't have a severe enough infection to produce an immune response. I've since come to believe that I'm already genetically equipped with an immune response that effectively takes care of covid. One example is that I have SNP rs10774671(G;G), which is the best-case scenario for the protection discussed in the study from the OP. 

I am unsure if I produced any antibodies from getting vaccinated. I never checked. You've piqued my interest, and I will check for antibodies if I get a booster. It's already been several months since I received my second dose, and I suspect any antibodies I may have produced have likely already faded.

As for why someone would not produce antibodies from vaccination or infection, the most commonly cited reason is that they are immunodeficient. Although those I know with an immunodeficiency were able to produce robust antibodies from the mRNA vaccines. Genetics, past infections (not necessarily from covid), immune system status, age, health, and nutritional status have all been linked to non- or hypo-responsiveness to other infections or vaccines.

a reply to: marg6043



Perhaps the complete opposite of a problem is happening. Innate immune system

Seen some studies where people shared a cabin with a positive case on a ship for 3 weeks and got nothing - So virus must have been stopped because they would have had to had a infection.

There are some people that have super antibodies so logic would determine that we are all different. New Studies Find Evidence Of 'Superhuman' Immunity To COVID-19 In Some Individuals

I am very interested in this issue, I wonder how many other people are with this same issue when it comes to how the body reacts to viruses and vaccinations.

But would not this people be getting covid and been very sick? or sick to any other disease, but these two individuals are healthy with not other health related issues.

a reply to: marg6043

interesting thing to think about blood. how many types?

Millions

originally posted by: tamusan
a reply to: rickymouse

Are you sure that Ancestry didn't genotype rs10774671 for you? I just checked and they did for mine. I've used livewello, but like promethease.com better.

That snp is an AA, but it states it is ambigious which usually means there is little evidence to show it effects anything with an AA. AA is the most popular one, but when something is popular it does not mean it is the good one. About sixty percent of the population has the AA according to what I read. It is supposed to make you more susceptable to rna viruses.

But that makes no sense, I never get a very bad virus. There may be another way of making an enzyme that does the same thing, one that cancels out the negative of this enzyme reduction. I looked at a gene app, first, a genset which did not include that snp for some reason. I must make a different variation of an enzyme that does the same thing. I do not have any of the diseases listed on the snp except for autoimmune disease family history and RA in my family. I definitely do not have a cytokine deficiency, my body attacks everything fast so far and the cytokine storms from vaccines shows a major increase in over stimulation if something is injected in my body. When you study and read all the stuff I have on the risks of the epigenetic factors you see a pattern emerge, changing one enzyme often opens the door somewhere down the line for the creation of another enzyme to balance things. But sometimes that other pathway is not created in conjunction with the snp that is not working right.

It is like the diamine oxidase deficiency, there is another enzyme that can also detox histamines, but if you eat foods high in other tyramines, that enzyme will be deficient to detox both. A deficiency in both of those enzymes can cause a lot of problems if you eat lots of tyramine foods...Histamine is actually one of the tyramines, others are putramine, cadaverine, and other powerful amines in that class.

From my research on their research, I have found that much of what they have found is just an increase of risk factor in some people. Even the A allele in this case in some other research in two other countries showed an opposite effect to the Mexico study. The possible reason could be the diet is different in those cultures of the other countries, enzymes can be consumed in foods to make up for the inadequate enzyme, cultural diets often make up for genetic variant differences and cancel out the negative effect. There are enzymes and food chemistries that can make up for a loss of enzyme. I talk about some of these foods and the heat stability of the enzymes quite a bit. Ovum from eggs, cooked over easy can deactivate this virus, so can an enzyme still active in milk as long as the pasteurization is below one hundred seventy degrees. So can the albumin in meat juice, the runny juice is gelled up by the loss of enzyme when heated, medium or rarer still has this enzyme. There are also plant enzymes that can help to deactivate viruses. I have mentioned these too. There are also foods that inhibit P450 enzymes that change ratios of enzyme creation in the body, one of the most well known ones is in grapefruit but there are other foods with similar but also a little different chemistries that can alter enzyme creation or destruction in multiple ways. This kind of stuff is the fuel for pharmacology research and drug developement.

That was tough for me to get through, but it sounds like a roll of the genetic dice. Do you propose getting a genetic test to determine our risk of getting a deadly case of COVID if infected? I guess I'd like to know if I'm doomed due to my genetic make-up.

I'm not sure of the point unless there is some way like gene therapy to protect those that have this genetic characteristic.

Wait. Ricky just answered that.

a reply to: rickymouse

Hundreds of interferon-stimulated genes have been discovered so far. There will also be a lot of other genetic characteristics that can predict an individual's covid outcome, but I believe they must be considered in conjunction with environmental and lifestyle factors. When time permits, I'm going to write an exhaustive thread that addresses all of the genetic elements that are currently known. As it seems you are aware of, dna analysis predicts a possible outcome, yet what is anticipated frequently does not materialize. I shouldn't have been so definitive in my OP. The thread was mainly intended to address an accusation that was thrown at me the other day.

According to what I've seen, the non-African haplotype that carries the G allele is descended from Neanderthals. The ancestral G is the majority in Africa; however, a small percentage of people are A, which was passed down to the Eurasians. It's also true that East Asians have low G allele frequencies as well. The Yakuts are among those who lack it, so perhaps this was ancestral to the Siberians? The Americas are home to three of the four populations that lack copies of the G allele. The Maya people have extremely low G allele frequency, and they are known for having European admixture. Peruvians had the highest frequency of the A allele. Peru has the world's highest C19 death rate, and the prevalence of A indicates that a large proportion of people will be AA. These statements derive from my analysis of Anders Bergstrom’s HGDP whole-genome data. My access does not come from a shareable source, but I believe there are free public access points. If you want to dig into this for yourself and can't find public access, speak up and I will try to find one for you.

a reply to: MichiganSwampBuck

I don't recommend diving into your genetics for health reasons unless you are particularly interested in these things. All it would do is cause anxiety for those who are prone to worry. Usually, it is not just one gene, but several that are needed for a predicted outcome to manifest. There are also often environmental and lifestyle factors. I chose this study because it is based on interferon, which is a well-known part of the innate immune system. As for the point of the study, it will likely lead to the creation of a medication that could better treat covid. There is an interferon-based therapy for multiple sclerosis, for example, that was the product of similar research.

a reply to: tamusan

You have been doing research. I feel better, I get OCD when I research things too, verifying if there are flaws in the interpretations and look for different cultural food consumption and ancestral eating habits.

When I got the ancestry done and got the promethius and livewello apps, I spent at least a year of eight hours or more a day researching how the stuff is interpreted and what it actually means. I got a bonus when I bought the the five dollar each promethius life time updates apps and I bought for everyone in my family and I even got it for my ex wife and for my two son in laws. With that I got the free My Heritage Ancestry when they merged, so we all have the relatives we can search in the My Heritage site, they are doing more with the lineage, that is where I found I have one point seven percent inuit genes on my fathers male genetics...it did not transfer to my two daughters, it is paternal. That inuit genetics also includes three percent of Finnish and other scandinavian people and some groups in Siberia that share those genes. I do not know if the double A is related to that.

I can tell you one thing about your thought about the extensive thread, in the time since 2014 when I got the initial genetic data from ancestry, what has been altered in the interpretation of the gene snps has changed a lot. They are learning more and more every day on how to interpret that info. Some of the initial research is still being used in the interpretation, but it is evolving fast on how to apply this stuff. I am actually impressed by the progress, but also understand it will be years before it is completed. I initially figured it would take five years, but I was mistaken, maybe when they hit the twenty year mark from what I initially studied this, the bugs will be worked out pretty well. I only spend about ten hours a month now updating my knowledge about this, a lot of the initial research I did was trying to figure out how to read and interpret what they were saying correctly, something that the majority of the people using the genetic data to judge disease risk should be doing before they start quoting this stuff to the public. Just like the brca genes, diet has a lot to do with the risk factors of breast cancer from that, but still that actually has a higher risk factor for about five percent of the breast cancer cases, only five percent of all breast cancers are caused by Brca genetic risk, and some of those Brca cancers have more to do with diet effecting the gene than the gene itself. I would not advise a woman to get her breast and or ovaries removed because they have the gene.

I did take a couple of classes to do with cancer and genetics through Future learn for free, mostly to try to understand how to communicate with those in the field. I did learn some stuff from those classes, but also conveyed what I learned in the chat too. I had some teachers get back to me, I opened up their minds to look at things differently, and they did some research that led to them verifying my stuff. Which they relayed to others in the class. It was definitely worth taking those twenty six medical classes there, I had no knowledge of how to approach medical professionals with my knowledge I found on my own....I did know how some doctors envisioned things, but not specialists in their fields, Now most classes have a charge even to get a completion and grade, since I do not need the documentation, I am not going to spend the money to get proof I took a class.

It is nice to find someone with the same desire to learn about genetics. I try not to go over people's heads with information, it can make them avoid you if you use too many scientific words, I try to translate things into layman's terms, but not all things can be translated, I have to use medical and chemical terms sometimes. I can understand this stuff, but I spent a real lot of time learning how to do it and apply it properly and translate it. I do not just want to talk to specialists in medicine, I want to try to teach others what it means. I do not like to intimidate people unless I have to in defense and even then I would rather back down and let professionals believe they are right sometimes, because maybe it will open their eyes to do more research into what I am talking about and find better ways to help people if they incorporate it into their practices.