Researchers find new coronavirus strain 'more contagious', potentially impacting COVID-19 vaccine search - ABC News
abc.net.au/news/2020-05-06/new-coronavirus-co...
abc.net.auPosted May 6, 2020, 6:58 AM UTC
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abc.net.au"The research, which has not been peer-reviewed"
Jumping the gun a bit there
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On the plus side, we're running a live experiment on societal lockdown, with the USA and Brazil on one side, and the countries with sane governments on the other.
The evidence appears to be piling up ...
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Live somewhere other than Earth
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Get better parents
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USA is just showing it’s true colours, it has lives that they are willing to sacrifice. Just as they have in wars etc. A million Americans dying under a private health care system is by design. USA is bought and paid for by big businesses, who need American workers working.
It is an interesting experiment because if you take the ethics out of it, there’s a real chance that economically this will be beneficial. If the USA maintains propaganda, power and control they will kill a lot of people but keep their economy ticking over with the population under control. It could go in an alternate direction if the propaganda fails and people protest.
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Lol they called it the G-string, I mean, g-strain.
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There are other ways of blocking the transmission of such viruses that can work in conjunction with vaccines and distancing measures, as well as enhance PPE functionality, but which have the additional benefit of not being affected by the virus mutating. The concept is explained here along with references to relevant existing research and methods: https://dsmatthews.blogspot.com/2020/04/covid-19-solution-changing-rules-of.html If anyone can be bothered to take the time to read all of that and thinks they understand it fully I would welcome contributions and or constructive criticism.
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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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Also, we cannot ensure that the proteins will fold properly in prokaryotic (bacterial) cells to ensure that they are a function target for the spike protein. The post translational modifications needed for the three dimensional folding of proteins are very different in bacterial cells to mammalian cells.
Simply administering a recombinant form of the human ACE 2 receptor (rhACE2) would be just as viable an option.
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Simply administering a recombinant form of the human ACE 2 receptor (rhACE2) would be just as viable an option.
Yes, and that brings up another issue with both ideas - ACE2 has enzymatic activity, so dosing people up with extra ACE2 whether in a free form or attached to bacteria is likely to cause serious side effects (e.g. dangerously low blood pressure).
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In saying that, it is likely that the expression of ACE2 in virally infected patients is significantly down regulated. As virus binds to the receptor it is internalised and often decreases. Hence it’s is possible that a disruption of the ACE/ACE2 axis is one of the factors causing pathology especially as high mortality rates can be seen i those whereby ACE2 is already compromised (hypertensive people and diabetics).
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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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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.
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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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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I'm not going to claim to understand it fully but I will immediately hoarde yoghurt just in case you're right ;-) so glad people are thinking outside the box btw (or the tub as it were).
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:-) Thanks.
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If you want a reason to not let this thing spread through a few extra hosts...
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If the research holds up to peer review it’s already the dominant strain in Australia. Current measures to contain it clearly work.
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Yeah I mean it's a reason you don't want millions of people getting it giving it further opportunity to mutate. Consider how many people were infected when they started researching this strain, now imagine how many opportunities for mutation it's had in places like America.
Yeah will be interesting to see if it holds up and what implications it has.
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Actually, typically mutations lead to less dangerous strains as it selects for those more likely to be spread with symptomatic illness being a strong negative selector.
Also mutation mapping allows for identification of critical regions (which cannot mutate) thereby highlighting targets for drug treatment and vaccine development.
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Whilst that is true for more deadly viruses, it may not actually be true for COVID. Since the virus is not as deadly (IFR most likely <1%), it is foreseeable that it could mutate into a more deadly virus and still spread easily. Not saying it will, but it is still possible
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And yet we are about to abandon those measures.
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Speak for yourself. I’m in Victoria
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Yes, Andrews has been great. But how long will he maintain measures under federal pressure.
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Let’s just keep everything the way it is for the one, two or even more years it will take for a vaccine, yes very sustainable.
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I read about the more prevalent second strain at least two months ago. It looks like we’re running short of new news.