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I've been thinking about the nature of security in biology. How do you keep enemies out when you are guarding something valuable like an oasis or your heart/bra

by pgt 7y ago

I've been thinking about the nature of security in biology. How do you keep enemies out when you are guarding something valuable like an oasis or your heart/brain? Well, we can install layers of access control like cell membranes which apply access control. We can cordon off the nuclear power plants (like mitochondria) with a "dumb" API that produces energy in return for nutrients and avoids "smart contracts". In the medieval sense, we can dig a moat and install a drawbridge. Bridges adds latency, but at least you can retract them during wartime. But the enemy is pretty clever, so they carry long ladders across the desert that can span the moat. So you add a winding cave before the moat so the ladders don't fit. But then they wisen up and pay spies behind your lines to lower the bridge, which is analogous to hijacking your immune system, or they invent a folding ladder, and so on. But none of this helps you if your enemy can consume you at a macro scale by swallowing you whole. So complex species tend to grow larger or add multiple layers of specialised topology (organs) with disposable individuals - not to mention growing their societies. I suspect there exists a "Shannon Information Theory of Survival" that can guarantee a defensible strategy as long as you can inject sufficient variance into the environment (high pressure, low pressure, vacuum, hot, cold, acidic, etc.) so that it would be more costly for an attacker to usurp you than to forge an alliance.

Erlich_Bachman 7y ago
It warrants to be careful with analogies though, because no matter how clever or graphic or seemingly appropriate they might seem, the point of analogies is simply to make our human mind understand complex processes better - they don't necessarily provide any new information about those processes or what would work to affect those processes and what would not. Empirical evidence is what is interesting and applicable in practice. Analogies can be used after that evidence is already collected, to put in a biology book to make students sweat less. But trying to use analogies to make up new information is over-intellectualizing - rarely a wise thing to do.
- feanaro 7y ago
  > But trying to use analogies to make up new information is over-intellectualizing - rarely a wise thing to do. Is it? It seems like analogies can often point into the right direction to look at. Of course analogies are not sufficient and you do need to do the actual empirical work, but it also seems a bit unwise to discard their ability to detect similarities. The only reason you can make a good analogy is because there is an underlying shared abstraction .
pazimzadeh 7y ago
In the large intestine, mucus is your moat (Fig 3D). https://www.pnas.org/content/105/39/15064 https://www.pnas.org/content/105/39/15064 The key is that you can't really stop the bacteria from coming in. You have to actually feed them so that they don't get desperate enough to blow a hole through your defenses. But what you feed them is a complex mix of polysaccharides that take take a long time to chew through. https://www.nature.com/articles/nature23292 https://www.nature.com/articles/nature23292 Your variance hypothesis is basically correct. The goblet cells of the epithelium express ~20 enzymes that decorate the protein backbone of mucus with six O-linked sugars in such a way that the composition is never the same, because of all the different types of linkage combinations possible, which means that no one bacteria can sweep through and gain permanent access. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4982847/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4982847/
- pazimzadeh 7y ago
  I was looking for this reference yesterday but couldn't find it: Cooperative Metabolic Adaptations in the Host Can Favor Asymptomatic Infection and Select for Attenuated Virulence in an Enteric Pathogen https://www.ncbi.nlm.nih.gov/pubmed/30100182 https://www.ncbi.nlm.nih.gov/pubmed/30100182
COGlory 7y ago
What you will actually find is that pathogens are generally pretty bad at what they do, and nature selects against them because they tend to kill their host too quickly. There are many organisms that infect but do not cause symptoms that propagate much more genetic material that pathogens. Similarly, we don't want to be too defensive. It's expensive, and the more complex our immune systems become, the greater the chance of autoimmune disorders. The more energy we spend protecting ourselves, and not growing. Therefore we will never develop perfect immune systems, and pathogens will never be perfect killers. The arms race analogy does a poor job of illustrating that in actuality, host-pathogen interactions are something of a dynamic equilibrium at this point.
MayeulC 7y ago
That would be a very interesting thing to explore indeed. I suspect we could already see some of it appear with some simple cellular automata. We could probably get many insights from it, and better predict issues such as resistant germs. > with disposable individuals And this is also something interesting: if an individual is too resistant, you risk propagating a disease to a large portion of the population. If each individual is too weak, you risk taking down the whole population. There are probably some evolutive pressure at play: a population with a rampant disease (a parasite, for instance) might be less competitive than another one that sheds its infected members.

by pgt 7y ago

Erlich_Bachman 7y ago

It warrants to be careful with analogies though, because no matter how clever or graphic or seemingly appropriate they might seem, the point of analogies is simply to make our human mind understand complex processes better - they don't necessarily provide any new information about those processes or what would work to affect those processes and what would not. Empirical evidence is what is interesting and applicable in practice. Analogies can be used after that evidence is already collected, to put in a biology book to make students sweat less. But trying to use analogies to make up new information is over-intellectualizing - rarely a wise thing to do.

feanaro 7y ago
> But trying to use analogies to make up new information is over-intellectualizing - rarely a wise thing to do. Is it? It seems like analogies can often point into the right direction to look at. Of course analogies are not sufficient and you do need to do the actual empirical work, but it also seems a bit unwise to discard their ability to detect similarities. The only reason you can make a good analogy is because there is an underlying shared abstraction .

pazimzadeh 7y ago

In the large intestine, mucus is your moat (Fig 3D). https://www.pnas.org/content/105/39/15064 https://www.pnas.org/content/105/39/15064 The key is that you can't really stop the bacteria from coming in. You have to actually feed them so that they don't get desperate enough to blow a hole through your defenses. But what you feed them is a complex mix of polysaccharides that take take a long time to chew through. https://www.nature.com/articles/nature23292 https://www.nature.com/articles/nature23292 Your variance hypothesis is basically correct. The goblet cells of the epithelium express ~20 enzymes that decorate the protein backbone of mucus with six O-linked sugars in such a way that the composition is never the same, because of all the different types of linkage combinations possible, which means that no one bacteria can sweep through and gain permanent access. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4982847/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4982847/

pazimzadeh 7y ago
I was looking for this reference yesterday but couldn't find it: Cooperative Metabolic Adaptations in the Host Can Favor Asymptomatic Infection and Select for Attenuated Virulence in an Enteric Pathogen https://www.ncbi.nlm.nih.gov/pubmed/30100182 https://www.ncbi.nlm.nih.gov/pubmed/30100182

COGlory 7y ago

What you will actually find is that pathogens are generally pretty bad at what they do, and nature selects against them because they tend to kill their host too quickly. There are many organisms that infect but do not cause symptoms that propagate much more genetic material that pathogens. Similarly, we don't want to be too defensive. It's expensive, and the more complex our immune systems become, the greater the chance of autoimmune disorders. The more energy we spend protecting ourselves, and not growing. Therefore we will never develop perfect immune systems, and pathogens will never be perfect killers. The arms race analogy does a poor job of illustrating that in actuality, host-pathogen interactions are something of a dynamic equilibrium at this point.

MayeulC 7y ago

That would be a very interesting thing to explore indeed. I suspect we could already see some of it appear with some simple cellular automata. We could probably get many insights from it, and better predict issues such as resistant germs. > with disposable individuals And this is also something interesting: if an individual is too resistant, you risk propagating a disease to a large portion of the population. If each individual is too weak, you risk taking down the whole population. There are probably some evolutive pressure at play: a population with a rampant disease (a parasite, for instance) might be less competitive than another one that sheds its infected members.