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COVID-19 Solution - Changing the rules of the game of life.


Please evaluate and disseminate this information as widely as possible.

The COVID-19 virus is, in abstraction, just a finite automata propagating through a substrate and that substrate is humanity, most mitigation efforts center around futile attempts to partition off parts of the substrate, other more effective but risky strategies involve modifying the behavior of the substrate to make it hostile to the virus. Great work guys but you got lost in the details and missed something very obvious.

Make humanity just a small part of the substrate and make most of it incapable of replicating the virus.

So how can we do that?

Genetically engineer a lactobacillus bacteria that is ubiquitous in the environment and on human mucosa so that the bacteria expresses the ACE2 (or any other required viral target!) gene so that the virus attempts to merge with the bacteria as if it was a human cell. The bacteria will however be engineered to immediately destroy the conserved parts of the viral genome. You can make the organism safer by also making it dependent on an artificial amino acid that does not exist in nature.

This lets you brew up a self replicating and sustaining, yet controllable, bioshield that can cover surfaces in buildings, public spaces and on the bodies of humans including the areas that are targeted by the virus, the mucosa.

NB this system can help protect against any virus that enters via the mucosal route, and it also prevents those already ill from shedding so many viral particles via that same route.


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Comments

  1. If you are wondering why a probiotic bioshield solution is required (outside of the third world) you may wish to consider the follow risk amongst a cohort that is known for their inability to modify their behaviour adequately to ensure good hygiene. https://www.nature.com/articles/s41575-020-0295-7

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  2. One way of looking at this type of technology is as a form of externalised and programmable immune system. In this role it is able to offer protection to those people who cannot mount and adequate response with their own immune system, the elderly and the immunocompromised such as transplant recipients.

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    1. You could also look at it as a form of "firewall" for lifeforms as it helps to block the flow of maleficent genetic information across the mucus membranes in both directions. It is not a question if it can work, rather it is a question of what number of bacteria per square mm of mucosa will reduce viron survival to levels so low that its replication number means that it becomes nonviable. It is not unlike herd immunity where you are recruiting bacteria into the herd for the purpose of boosting the total number of hosts that are not vulnerable to the virus.

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  3. The following is a candidate to satisfy the need to "destroy the conserved parts of the viral genome"

    Development of CRISPR as a prophylactic strategy to combat novel coronavirus and influenza https://www.biorxiv.org/content/10.1101/2020.03.13.991307v1

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  4. A basic introduction to the COVID-19 virus and how it works can be found here, https://www.nytimes.com/interactive/2020/03/11/science/how-coronavirus-hijacks-your-cells.html N.B. the gene engineering required to produce a vaccine in large quantities is similar to that required to satisfy the need to "Genetically engineer a lactobacillus ... so that the bacteria expresses the ACE2 (or any other required viral target!) gene"

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    1. For a more advanced discussion see: "The cell biology of receptor-mediated virus entry" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246895/

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  5. The need to be able to satisfy the need to be "dependent on an artificial amino acid that does not exist in nature" is described in Recoded organisms engineered to depend on synthetic amino acids https://www.nature.com/articles/nature14095

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  6. One example of a related idea actually used in practice, "Fighting malaria with engineered symbiotic bacteria from vector mosquitoes" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412027/

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  7. I haven't time to do a complete rewrite that incorporates these nots, yet, so I will keep adding them here but there will be a version two of this document at some point in the future. These comments will include replays to people's questions that have been put to me elsewhere so that I can capture the ideas.

    Vaccines for COVID-19 are a long way off and will not ever work for several groups of vulnerable people, that is why I proposed the engineered probiotic bioshield, it uses a receptor decoy to trap and destroy the viral particles and if the virus mutates to avoid the decoid you have also forced it to become unable to infect humans. Neat huh? The bioshield method also helps protects against ALL viruses that are transmitted via the mucosa. Mind blown yet? Another nice feature that is has is its dependence on a artificial amino acid/s, this means that you can deploy it and it will just die off, unable to survive in nature, then you deploy the next version which uses another amino acid, you cycle these one after another (3 or more) so that you have continuous protection but your solution cannot live long enough to be problematic and it is easier to roll out upgrades to its genetics. Later you can add additional genetic material to have the bioshield bacteria shed bacteriophages that also attack pathogenic bacteria too. What this means is that it eats pathogenic viruses, digests their components then uses the raw materials to produce other viruses that only attack "bad" bacteria all the while being unable to survive without humans supplying it with its essential artificial amino acids. None of this requires novel biotech that has not already been studied! That is the part that astounded me while I was researching the feasibility of the idea! But there is one problem, old people will not die as easily as they do now, so once cancer is conquered you are left with large number of very long lived people with dementia etc.

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    1. There is no profit to be made, this is about saving lives and is open source. Nothing is injected. It is a bioshield that can have regular genetic "software" upgrades. It is a programmable externalised immune system layer. The development costs of each new upgrade is potentially significant, but the rollout across the globe will be as cheap as sending inoculant for people to brew up locally at very low cost. The virus trap works on its own but you may as well have it recycle its viral victims into weapons against "bad" bacteria. However this phage feature is just a nice secondary feature, not required for COVID-19 or any other similar viral diseases.

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    2. It isn't a product it is a lifeform, it builds itself, with minimal help from humans once it is designed. That is one of its key features. A single liter of cell culture shipped to a country can scale up to national level coverage within weeks and being lactobacillus you can grow it on as many different substrates as there are existing fermented food types. i.e. It can grow on fruits and vegetable wastes from the food industries. Make it at home like you brew beer, or in the megaliters in a factory as it works at any scale, so in any nation rich or poor. The only limiting factor is the exotic amino acid needed to control its ability to grow and that can be engineered to be minimised, just enough to get the job done and then without it the bacteria is living on borrowed time, according the the previously mentioned time-table. It is the Linux of artificial immune systems. Nobody will get rich off it, yet humanity will flourish because of it so the entire economy will boom and people will get rich off that.

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    3. The ability to upgrade the "genetic software" of a protective system such as the EPS is highlighted by the recent finding which shows that COVID-19 has potentially a second route of attack against immune cells. In the following case a second lure receptor can be added to the surface of the EPS. See: "SARS-CoV-2 invades host cells via a novel route: CD147-spike protein" https://www.biorxiv.org/content/10.1101/2020.03.14.988345v1 However this may not be required except for the risk of causing the evolution of a COVID strain that only targets CD147 if all ACE2 biated strains are lured to their destruction using a single recptor lure version of EPS.

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  8. Many people make the mistake of thinking that the coronavirus is solely a respiratory pathogen when the truth is that it is involving all of the mucosa that express ACE2 (https://www.ncbi.nlm.nih.gov/pubmed/15141377). The evidence was well documented during the original SARS1 outbreak. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7112410/ https://www.nature.com/articles/s41368-020-0074-x

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  9. One interesting option is to have the EPS (Engineered Probiotic Shield) cells express immunoglobulin, "Efficient expression of full-length antibodies in the cytoplasm of engineered bacteria" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4560801/ However that would need to be adapted from the E. coli example to work in the EPS lactobacillus.

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  10. If the EPS was deployed and became ubiquitous around human habitats then the following risk is also mitigated. As well as Influenza house flies may spread Nidovirales, and that family includes Coronaviridae (COVID-19) See table 4 here --> https://link.springer.com/article/10.1186/s42269-019-0111-0

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  11. The "engineered" nature of the EPS has raised concerns from a small number of individuals however if you examine the literature it has been practiced and uncontroversial since at least 2009 when "Immunomodulation by genetically engineered lactic acid bacteria." was published, https://www.ncbi.nlm.nih.gov/pubmed/19482589

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  12. In memorandum. John H. Conway, 1937–2020
    https://www.math.princeton.edu/news/john-h-conway-1937-2020

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  13. One risk involved in vaccinating against COVID-19 or relying on a population developing natural immunity is that there are mechanisms that could make things worse during subsequent exposures to the virus. See  *Antibody-dependent enhancement of SARS coronavirus infection and its role in the pathogenesis of SARS* https://www.hkmj.org/abstracts/v22n3%20Suppl%204/25.htm Similar mechanisms are described in *COVID-19: immunopathology and its implications for therapy*  https://www.nature.com/articles/s41577-020-0308-3

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  14. For a related idea that is more inert (and much more expensive), not living yet able to lure and trap specific viruses expressing particular spike proteins see "Beyond natural antibodies – a new generation of synthetic antibodies created by post-imprinting modification of molecularly imprinted polymers " T. Takeuchi and H. Sunayama, Chem. Commun., 2018, DOI: 10.1039/C8CC02923G. I do not favour this idea at all as it has a lot of drawbacks that do not outweigh the perceived safety benefits. I have included it for the sake of completeness and as evidence that the idea is broader than people imagine and therefore should not be dismissed completely out of some unfounded fear of GMOs.

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    1. Yet another inert and expensive idea that may also be dangerous if it requires injecting into the blood stream. https://le.ac.uk/news/2020/april/17-decoy-protein-covid-19?fbclid=IwAR3IdmgBbxVMKcqjTUatGkY4Z9l-mbuLAV7udANFjrMmvVp_JTubKDhmE_A

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  15. Interesting research that may be related, are we looking at a natural occurrence of some aspects of the above ideas? "Evaluation of the efficacy of Lactobacillus plantarum HEAL9 and Lactobacillus paracasei 8700:2 on aspects of common cold infections in children attending day care: a randomised, double-blind, placebo-controlled clinical study" https://link.springer.com/article/10.1007/s00394-019-02137-8

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  16. Probiotics, mainly lactic acid bacteria (LAB), are widely focused on gastrointestinal applications. However, recent microbiome studies indicate that LAB can be endogenous members of other human body sites such as the upper respiratory tract (URT). Interestingly, DNA-based microbiome research suggests an inverse correlation between the presence of LAB and the occurrence of potential pathogens, such as Moraxella catarrhalis, an important URT pathogen linked to otitis media, sinusitis and chronic obstructive pulmonary disease. https://www.ncbi.nlm.nih.gov/pubmed/29633637

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  17. Since a healthy adult breathes more than 7000 l of air a day, the upper respiratory tract (URT) is constantly bathed in airflow from the external environment. Along with the air, 104–106 bacterial cells per cubic meter of air are inhaled per day. "The microbiome of the upper respiratory tract in health and disease" https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-019-0703-z

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  18. Video: "Joining 3.5 Billion Years of Microbial Invention | Craig Venter" Long Now Foundation. https://www.youtube.com/watch?v=OWX_12eA_qQ

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  19. I got some good questions from a Redditor, there they are and my answers follow them.

    from FreqquentFlyer via /r/australia

    Sadly cannot see this being a viable idea, at least with our current technology and biological knowledge.

    Most receptors on human cells, including those targeted by viral cells, have a physiological role - e.g. ACE2 is involved in blood pressure regulation. If your genetically engineered bacteria is given to people to essentially outcompete human cells for virus binding, then will it also interfere with the action of other (normal, physiologically necessary) substrates that bind to ACE2 on human cells?
    How will the bacteria be "engineered to immediately destroy the conserved parts of the viral genome"? And how can you guarantee this will not just drive evolution of the virus? We don't understand everything about this virus yet, remember. On top of that, if for example the bacteria use some enzymatic way of destroying the viral genome, how do we ensure this enzyme wouldn't also be dangerous to human cells (e.g. if it were released onto human mucosal cells when the bacteria die)?
    Do we know enough about systems biology and genetic engineering to safely modify bacteria as you describe and release it "into the wild" without unintended consequences? There's still a lot we don't know even about something as "simple" as the lactobacillus genome. We don't want some kind of environmental disaster like what happened when cane toads were introduced to Australia. And the last thing we want is to create another pathogen on top of the pathogen we're already having so much trouble with.
    Genetically modified bacteria tend to reproduce poorly outside strict lab conditions where they're the sole species in a tube of food in a comfy incubator. They're simply less 'competitive' than natural species that have evolved to survive on real environments. How will you ensure the bacteria are not out-competed by other species so they can actually survive on the surfaces you want to apply it to? And related to this: if you do make these bacteria hardy enough so they can survive, how do you know you're not destroying the micro-ecosystem that already exists on these surfaces - again with possible unintended consequences? This would be especially important if you're thinking of administering it to humans, where maintaining a balanced microbiome is important for health.
    Another issue with bacterial survival on surfaces: If the bacteria is made "safe" e.g. by depending on an artificial amino acid, how do we supply those surfaces with enough of that amino acid? Is the amino acid stable in the environment? Is the amino acid widely available and cheap enough to continually reapply when it's consumed by the bacterial layer? What other nutrients do the bacteria rely on - and do all these same questions apply there too? How is this going to work for human mucosa?
    A more practical issue: Bacterial colonies and biofilms are sticky and kind of gross. Think of the slime on swimming pool pipes and the gooey colonies on agar plates. How do we apply that to stuff like common-use surfaces and PPE?

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    1. Thanks for your questions and observations!

      The references I have found so far suggest that our knowledge and technology is actually sufficiently advanced and has been so for perhaps 10 years or longer. The more I look the more I am astounded by what has been proven to be possible.

      The lactobacillus is not resident within the blood so it will not mess with your internal physiology as directly as you suggest and it can't help you once the virus is in your bloodstream, except that you can't shed particles via your mucosa and reinfect yourself so your viral load will be indirectly lowered.
      The issue of the method of destroying the virus and not being impacted by mutation is covered in the comments below the text, with references to relevant research. There are multiple options there including what bacterial already do naturally and what researchers have proposed. That part may be subject to a patent, I hope not or that they are nice about it!
      The risk of unintended consequences is also covered in the text and the comments, it can't survive without a supply of an unnatural amino acid. This is well established tech to allow engineered e coli to be used as chemical factories.
      The "reproduces poorly" would be a feature and tuneable, in fact you can make it so that it does not reproduce at all if you don't feed it, see point 3. The idea is that it dies off totally once the job is done, when the viral replication rate is driven so low that it becomes extinct as SARS1 did.
      Surfaces are regularly cleaned and made sterile and still should be, except the last procedure could be a light spray of an inoculant to reestablish the bioshield. But you touching them would add it too, you would be spreading the shield while it is on you and active. This links the shield's distribution to the same sites that the virus would be as it is the same process, human activities. I actually think that is a pretty neat aspect of the idea, it uses an aspect of the problem to be part of the solution.
      No not all bacteria need form colonies that you can perceive and their numbers do not need to be that massive to protect you, you don't notice the ones that are covering you now do you? See the comments and references right near the end of the comments section, these bacteria really are ubiquitous already. Had you ever wondered why the virus is not surviving on cardboard for very long compared to cleanable surfaces, maybe it is because it is already covered in bacteria that just see virion particles as food. They do like to hide out on porous surfaces that hold moisture, an ideal home for bacteria compared to smooth plastic or metal.
      One other thing to consider, this protection does not need to be 100% effective to be a big help as it can work alongside current strategies, it is all about lowering the rate of viral replication. If I have the virus and the shield is on me I can't shed virions as much (they need to exit via the mucosa zone the bacteria live in), then what particles are shed need to get past the shield on surfaces, then finally the shield on another person further lowers its survival. Even at 20% effectiveness those three steps add up to a 60% reduction in transmission rates, then you add all of the other measures you are using. It all adds up!

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    2. from FreqquentFlyer via /r/australia

      It's true there are always amazing technological advances being made. But I can tell you from experience that unfortunately what sounds like incredible new advanced tech on paper doesn't necessarily work so nicely in reality. Especially in biotech, there's often a lot of fine-tuning required before something can really be as good as the theories suggest.

      The lactobacillus doesn't have to be "resident in blood" to have effects. Note that the cells naturally expressing ACE2 aren't "in blood" either - they're cells lining the lungs and gut, among other organs - and yet that ACE2 still functions physiologically. Also, many pathogens can cause disease without ever reaching the bloodstream. For example, these pathogens might release a toxin that can reach where the bacteria itself doesn't, including 'toxins' that are actually just the 'insides' of dead cells, released when the cells die (look up exotoxins and endotoxins); they might induce a damaging or inappropriate immune response; they might alter the local tissue function or microbiome; or all kinds of other mechanisms.
      The enzymatic way I described is one way that probably has the most potential (since it kind of exists in nature already - look up DNAses and RNAses). But that has its own problems, as I also described. I imagine other published/patented techniques would have their own advantages and disadvantages too.
      For points 3, 4, 5: You're juggling multiple problems here.

      Yes, the unnatural amino acid method to limit bacterial spread is well-established - but again, how easy is it to supply, how much does it cost, and will it even work outside of a lab environment (where it's usually added directly to the bacterial media i.e. "bacteria food")? You need to keep giving the bacteria this amino acid for it to survive, it's not a once-off dose.
      How well do you want the bacteria to be able to live on the environment you apply it to? If the bacteria have poor survival then it's essentially useless as soon as it's applied - it's too busy dying to protect you from viruses. Bacterial reproduction isn't the only problem here. In cell stress, protein production is one of the first things to go out the window, so they might not even express ACE2 any more. But if the bacteria are able to survive too well, then you're facing the same biohazard problems I described already. And this is only talking about applying the bacteria to surfaces - what about human mucosa?
      If you're considering a regular spray of low-survival bacteria onto surfaces after every cleaning, it'll probably be insanely expensive (genetically engineered bacteria aren't cheap and you'd need a huge supply of them). And will this spray contain bacterial media (including the unnatural amino acid) to help it survive? If so, what's the effect of human exposure to this media? And even if the media is harmless, the bacteria won't survive on human mucosa at all without it. If not (e.g. you'll just replace the bacteria with the next spray after they die), the bacteria probably won't work at all - see what I said above about being "too busy dying".
      For point 6: No, that's not why the virus survives poorly on cardboard. It's more likely due to the nature of the cardboard itself - coronaviruses have a lipid envelope, so they're likely not as durable on cardboard compared to non-porous materials (imagine a soap bubble on metal vs cardboard). Bacteria actually don't generally "eat viruses". Many species of bacteria can also survive just fine on metal and plastic (look up biofilms).

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    3. Note 1. Said bacteria is already in your lungs and on every other mucosal surface (see refs. in page comments, particularly the already proven effects against common coronaviruses) and the GM version needs only lure the coronavirus, it does not need to be able to be active in the sense that it is capable of catalysing the hydrolysis of angiotensin II. Otherwise your antibodies to the spike protein (natural or induced) would be also harming ACE2 function via competition. It only needs to allow the absorption sequence to be initiated, from that point the the uncoated virus is vulnerable to the usual digestion and recycling processes in the bacteria. They do "eat" anything that gets past their membranes that is not viable, those molecules just end up as parts or energy sources for the cells normal processes. That covers your point 2. the real issue it to ensure that the viral RNA is not viable once inside the bacteria, the rest is just cellular housekeeping.

      For 3,4,5 you have misunderstood the process completely and made strawman arguments based on that. The exotic amino acid accumulates in the bacteria when abundant in the environment (brewing time), otherwise it burns through its supplies (when deployed) then stops functioning (die-by-date). That is the point, you can tune that process. One way is to have competing drives, 1. accumulate AA into a protein structure and 2. break down said structure to liberate AA to be used elsewhere. In IT we call that a LIFO buffer . :-) The external input of AA into the cell keeps the process biased toward accumulation, then it switches to consumption. Imagine a timer fuse if that helps. You don't seem to understand how it functions from a biocybernetic point of view. It does not make the bacteria weaker than any other member of your microbiome, it just means that at some point it clears the "buffer" and dies. It is not a low or high survival bacteria, it functions fine, then crashes at a programmed point in time defined by a clock that is essentially its average metabolic rate. The price to design bacteria is higher, the price to grow bacteria is not high at all, particularly the type in question, this is pointed out in the comments under the text too. Did you actually read all of it? Production of exotic amino acids is not expensive and the amount in each cell is not as important as the turnover rate. Having it die is important (it is a feature and not a bug!) as pointed out previously this avoids mutations and allows you to use a sequence of versions so you have continual protection while allowing for the de-by-date, with the option to add new lures as an additional benefit (upgrades).

      Your point 6. claim seems rather bogus to me and contradicts what is known about "good" habitats for bacteria. Got a ref. for what you are thinking of? And stop mentioning biofilms they and their creators are not applicable and so are irrelevant. See the above point about "eating", if anything organic gets passed the membrane, by any means, and is not toxic to the bacteria, or viable genetic material, it gets cleaved and recycled, i.e. "eaten". Nom nom nom nom...

      And now for something else that you could have the bacteria do but it is entirely optional, make a non toxic fluorescent dye in response to detecting (ingesting) COVID-19. Would make a cheap UV lamp a great tool for affordably detecting a contamination event.

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  20. People with concerns about the above proposal should consider what sorts of methods and technologies are being deployed to produce a vaccine for COVID-19 anyway. The UK vaccine is a genetically engineered monkey virus that is live when injected https://covid19vaccinetrial.co.uk/about

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  21. I have had some rather naive comments with regard to the extent with which it is possible to implement formal logic and computing methods in living cells so I offer the following survey as an indicator, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4442017/

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    1. "Gene Circuits Empower Next-Generation Cell and Gene Therapies" https://www.genengnews.com/insights/gene-circuits-empower-next-generation-cell-and-gene-therapies/

      Also see the following for an idea of how advance DNA and molecular computing has become particularly in the area of implementing entire neural networks, https://scholar.google.com/scholar?q=related:7_CqJhENpuUJ:scholar.google.com/&scioq=Molecular+and+DNA+Artificial+Neural+Networks+via+Fractional+Coding.+arXiv+2020&hl=en&as_sdt=0,5

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  22. Here is a question that needs to be answered, do we have 1 virus but 2 diseases. Think about this, what is the difference between breathing it directly into your lungs and having it in the back of your nose then have that run down the back of the throat and into your stomach. With the first one the virus is kicking in the front door (directly attacking the lungs), in the second case the security guards (immune system) gets to see a few dead ones before the rest attack you. It may well be that all it takes to get a mild case is to have dead virus parts traverse a healthy gut, a form of immunisation vs full on infection. This also explains why Italian Drs died after intubating people, they breathed in a big spray of virus as the tube went in, this is a "normal" phenomena, so early on without PPE they were very vulnerable to getting a massive dose all at once. It may explain why kids will often get diarrhea rather than lung problems, they suck back and swallow mucus rather than blowing their nose, and in doing that they are using their gut to educate and moderate their immune systems. Are people who report diarrhea less likely to end up in the ICU than those with different symptom profiles?

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    1. Here is very clear evidence of what happens if the stomach is not as hostile an environment to the virus. Lowering acid levels makes things a lot worse. https://journals.lww.com/ajg/Documents/AJG-20-1811_R1(PUBLISH%20AS%20WEBPART).pdf

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    2. Yes it seems we do, perhaps even 6 rather than 2, see "Symptom clusters in Covid19: A potential clinical prediction tool from the COVID Symptom study app" https://www.medrxiv.org/content/10.1101/2020.06.12.20129056v1.full.pdf

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  23. Another way to enhance a bioshield bacteria is to have it also express neutralising antibodies against the virus. Again this helps people who can't mount an antibody response themselves, either at all or in a timely manner.

    https://science.sciencemag.org/content/early/2020/07/10/science.abd2321

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    1. "Potent binding of 2019 novel coronavirus spike protein by a SARS coronavirus-specific human monoclonal antibody." https://www.biorxiv.org/content/10.1101/2020.01.28.923011v1

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  24. A similar concept has already been proven to be effective in another viral disease.

    "An Exopolysaccharide-Deficient Mutant of Lactobacillus rhamnosus GG Efficiently Displays a Protective Llama Antibody Fragment against Rotavirus on Its Surface."

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4551240/


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  25. There is another way of producing a similar, but far less effective, lure for viral particles and the is a custom exosome that is decorated on its surface with the ACE2 or other viral targets (targeting peptides). As described in "Design strategies and application progress of therapeutic exosomes" https://pubmed.ncbi.nlm.nih.gov/30867813/

    This method can be used to construct non-replicating lures, or be the method by which the engineered lactobacillus makes the mucosa a hostile environment for the virus, by regularly budding off such decorated exosomes which may also contain antiviral components or mechanisms.

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  26. Yet another example of using modified Lactococcus to protect against viral infection.

    "Oral immunization with a recombinant Lactococcus lactis expressing HIV-1 antigen on GAS pilus induces strong mucosal immunity in the gut"

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4637245/

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    1. Similar work from the same year "Lactobacillus plantarum displaying CCL3 chemokine in fusion with HIV-1 Gag derived antigen causes increased recruitment of T cells"

      https://microbialcellfactories.biomedcentral.com/articles/10.1186/s12934-015-0360-z

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  27. Yet another reason why we need options other than vaccines, because they are useless in the immunocompromised and those patients are a breeding ground for mutant virus strains. They also seem to be suffering a long and cruel death from the virus, which is an ethically unacceptable situation to allow if we have options to help prevent it. https://www.sciencemag.org/news/2020/12/uk-variant-puts-spotlight-immunocompromised-patients-role-covid-19-pandemic

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  28. A version of this concept could also fight against fungal diseases by producing Mycoviruses

    DOI: 10.1007/s10096-010-0946-7
    Journal: European Journal of Clinical Microbiology & Infectious Diseases Volume: 29 Issues: 7 755--763
    Title: Mycoviruses: future therapeutic agents of invasive fungal infections in humans?
    Author(s): W. W. J. van de Sande; J. R. Lo-Ten-Foe; A. van Belkum; M. G. Netea; B. J. Kullberg; A. G. Vonk
    Publisher: Springer
    Year: 2010

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  29. This comment has been removed by the author.

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