> The idea is that when you get sick, your body just starts randomly throwing things at the virus to see what works, and eventually it finds something that “works”, even though it might not be the optimal solution.
> I suggest people pick up the book "Immune: A Journey Into the Mysterious System That Keeps You Alive 978-0593241318" as it does a much better job at explaining these systems then my short paragraph.
I read that book just a few weeks ago and I don't recall reading anything about the stuff you mentioned.
> There's also probably a balance between having an aggressive immune system and auto-immune disease.
This is the key. I’ve had an immunologist explain to me (over a bottle of wine, so my recollection is hazy) that our immune system is actually very very aggressive already and tuned within a few percentage points of being problematic.
> How exactly does the body figure out how to configure the variable part of the antibody so that it binds? Does it just try countless variations until it finds a match?
Not a biologist but IIRC, the body produces cells with a shuffled sequence of DNA. Then this specific cell produces one specific variant of antibodies, located on its surface. At this point the antibody is just a random sequence that matches with nothing.
If one day a virus (or anything else) happen to match with the antibody located on the surface of the cell, the cell will then multiply and most of the new cells will specialize into antibody-producing cells (released in the body, not remaining on the surface of the cell) and a small amount will not. The one who aren't producing antibodies are kept in the body for a long time, and they are here to provide quick specific response next time you meet the pathogen again (that's where immunity comes from).
So yeah, it's basically brute-force until a matching antibody is found.
> But duration is very difficult to reduce, because of the way the learning process of the immune system works. There's a bunch of sequential processes that occur sequentially.
I'm genuinely very curious for more detail about this. Can you describe what some of the processes are (or better, where I can go to learn about it)?
> The operative factor is how well your immune system recognizes the threat and produces antibodies, not how many virus copies were there originally.
These probably aren't independent, and are occurring at the same time. So while a very small amount of virus is replicating, the immune system is mounting a defense, slowing down that replication. The virus may never get to a significant amount (although the immune response might knock you on your ass.)
On the other hand, if you start with a ton of virus already, you'll be dealing with the immune response and the direct effects of the virus at the same time, and the virus may overwhelm or even limit the immune response.
> is there a department of immunology that takes over or even contributes.
Because we don't see the immune system as the organ it is. Which is odd that things like vaccines are effectively medicines for that organ.
But at the end of the day we still don't know 'that much' about the immune system because of its extreme complexity. It's still very difficult or impossible to target a bad acting immune response in an individual without disabling all the immune system (and yea, this puts you at a lot of risk).
I like the series that Kurzgesagt made on the immune system as a way to explain this complexity a little more simply.
> “For me, as an immunologist, the fact that there's this natural immune receptor that we didn't know about, that's lining our lungs and blocks and controls virus, that's crazy interesting.
> Edit: how does acquiring immunity fit in? If I get 60% of an infectious dose and then no further exposure until my body has dealt with that, do I get any immunity or does that only happen if I accumulate enough virus at one time to actually get sick?
Not an expert but I think I can handle this one.
> The model here would be that you have a virus accumulator (you), being filled by exposure events and drained by your immune system, and you get sick if the accumulator reaches some threshold.
This is a simplified model of the immune system, and in order to answer the above question we need to make it a little less simplified.
First, let's talk about the accumulator. It's not only being filled by sars-cov-2, but also by other viruses, foreign bacteria, etc. I don't understand well enough to say how that affects the threshold in our model so I'll ignore that for now. Let's represent all these as javascript objects.
As I understand it, your immune system has two main responses to infections: white blood cells and T cells[0]. They both work essentially by duck typing -- in our model, that's the shape of the js objects; irl it's the protiens exposed on the surface of the virus[1]. White blood cells match a much more general pattern, but are not very efficient compared to T cells. Your model only considers white blood cells.
T cells work a little differently. Your body constantly generates T cells that match random virus shapes. The newly-made T cells take a look through the accumulator and see if they match any of the objects. If not, they self-destruct. This is what hapoens most of the time, since the accumulator is cleaned out fairly quickly. But if they do -- say, when the accumulator has overflowed and now the virus is reproducing freely, so it stays around for a long time -- they start to clone themselves. Eventually, they clone themselves enough that they, with their higher efficiency, are able to remove all of the virus from the accumulator. When this happens, a few of them stick around for a while. This is immunity: even if you get hit with a big dose of sars-cov-2, you've got some T<sars-cov-2>cells hanging around from last time, which can handle the virus with increased efficiency (multiplying themselves[2] as necessary).
That is to say, a small amount of exposure over a long period of time is unlikely to generate immunity, since you never generate T cells to fight the virus.
[0] These are not the only parts, but they play a big role and generalize well to the two main parts of our immune system.
[1] Aside, you could, with a little fudging, extend this analogy to how viruses infect cells -- cells each have api endpoints, and the virus takes the shape of the regular payload enough to pass validation checking, but also has malicious parts to trigger remote code execution once inside the cell, so the cell turns around and starts spitting out viruses instead of its normal responses.
[2] Actually I do not remember what the mechanism is for this -- whether they multiply themselves or send a message back to the T cell factory to "produce more like me", at which point the T cell factory caches the blueprint, and that's the immunity, rather than any T cells themselves sticking around. Maybe someone with a deeper understanding of the biology can correct any nuances I'm
> People with high levels of immune resilience live longer, resist diseases, and are more likely to survive diseases when they do develop.
Pardon me, but isn't that stating the obvious? I mean tto say, your immune system protects you, and the better it does the less likely you are to succumb to disease, is what the immune system does. It's not like you're nervous system is going to beat back an infection.
> When you feel sick don't stay in bed, go for walks, a large part of your immune system is passive and rely on muscle contraction to work optimally.
Do you have a source for this? I haven't heard this before and genuinely want to learn more about it. A cursory Google search didn't find anything related to this
> 'we teach our immune system to fight diseases by showing them weaker versions'
This is a simplification of a well researched process which we understand and can read about. What the previous poster wrote was just speculation as far as I can tell, unless someone wants to post some reference about cleaning the brain and blood?
> The proper term is Immunological memory, and is a complicated subject I don't fully grasp.
It’s very obvious. You’re citing a popsci video while accusing others of falling prey to urban legends, and declining to offer references to the people asking for them.
Let me be unequivocal: all the points you’ve made are inaccurate (except #2), because you lack this fundamental understanding of the difference between adaptive and innate immunity, and the value of paratope diversity.
“Getting sick” (i.e. an infection reaching the point where it causes clinical symptoms) is crucial for the development of the adaptive immune response, whereby the body tries “randomized” antibody structures until it develops new ones that can bind to an antigen. Having a broad range of antibodies developed through this process, called somatic hypermutation, is important because your body uses prior antibodies it’s developed as starting points for developing targets against new antigens, so even for rapidly evolving targets like the flu, exposure to previous strains still can help stack the odds in the body’s favor.
> Some kind of ability to have contagious antibodies might be an actual improvement but the fact that we don't see that in nature tells me it has downsides that are difficult to see.
My biology education is a bit weak, but off the top of my head, autoimmunity being contagious sounds like a likely side-effect of contagious antibodies.
Straining for an analogy? Am I the only one who hated this quote from the article?:
"The idea basically is that your immune system
is occupied elsewhere. It would be like getting
the swirling ball of death on your Mac where your
operating system is doing something else rather
than opening the file."
This is a remarkably apt description of that part of the immune system. For anyone curious, see: https://en.wikipedia.org/wiki/T_cell#Development
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