One thing unclear from that is how how fast, if at all, accumulated viruses clear out.

Say you need to inhale 1000 of a particular virus to get its disease, and talking normally with an infected person gives you 200/minute, so it takes you 5 minutes to get the disease.

You can get that 1000 by talking 5 minutes with one infected person, or you can get it by talking 3 minutes with one infected person and then shortly afterwards 2 minutes with another.

But what if the gap between those two is longer?

I'd guess that the first 600 you got get into cells quickly and start reproducing, but there are few enough that your immune system is able to handle them. The reason you need 1000 is that is the tipping point where the viruses can reproduce faster than your immune system can handle.

If that's the case, then after you get that first 600, how many you need to get on the next exposure would be 400 shortly after the first, but as the time between exposures increases that would increase.

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 makes me wonder if my approach to shopping during this pandemic is wrong. I've been doing a big shopping trip every 3 or 4 weeks, as opposed to before the pandemic when I'd pop in to the store 3 or 4 times a week and only buy a few things.

Those big trips involve being in the store for an hour or more (and it's not linear--the time to fill my cart is linear in the number of things I'm buying, but checkout time goes up faster because organizing my stuff at the self-checkout becomes harder). If someone else in the store is infected, I could potentially be around them enough to also get infected.

The old small trips only involve a few minutes in the store. If someone else is infected I'm not going to be in there long enough to get an infectious dose from them unless they do something like cough near me. With my mask, and care to avoid other people who are not wearing masks, my realistic risk from an infected person is less than an infectious dose.

If my immune system can clear that out in a few days, then I should be good to go for the next short trip. As long as the prevalence of infected people in my community is low enough that I'm not going to get an infectious dose in a single short trip, this should be a safe approach.

Another question: suppose I get that 600 dose, and no more, so my immune system handles it fine and I don't get sick. Am I spreading the virus during this time, or do I only start spreading after I get an infectious dose worth of accumulated exposure?

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?

> 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