Being infected isn't a binary thing. There is a big difference from swallowing 30 Coronavirus particles from touching your face to breathing in 300,000 from someone coughing in your face.
If you're young the first is probably a mild cold while the latter is a trip to the ICU.
Part of bringing the virus under control is reducing the amount of particles people are exposed to so they have a better chance of fighting off the virus.
A very important thing is the topology of the infection. I had COVID last year and it progressed linearly over time, from the back of my nose(probably from a big water droplet I breathed)forwards(towards my nose) and downwards towards my lungs. I could measure the progress day after day.
It progressed linearly because the breathing system is a duct. Like a fire needs a boundary to expand, a frontier. It is not 3D but 2 dimensional.
You just can not do an exponential calculation, without taking into account the physical limits of the environment.
Just before entering the lungs I did beat it. I coughed for a month or so,specially for the irritation in my glottis, but nothing serious.
This year I got it again, the progress rate was very similar but my immune system reacted sooner.
What is interesting is that I did not developed antibodies, my antibodies test were negative but the PCRs positives. This means that my T cells were already fighting the infection.
That probably had something to do with living in China in the past and having developed immunity against SARS.
> That probably had something to do with living in China in the past and having developed immunity against SARS.
Only about 8000 persons have been recorded to come down with SARS. Were you one of them with a diagnosed case of SARS (10% fatality rate)? The vast majority of residents in China would have no exposure to SARS.
Alternative theory: you had something else for at least one of those reported illnesses, and your PCR test was a false positive. The rest is conjecture, anecdote, and speculation.
>If the virus population doubles every second then the person who swallowed 30 virus particles will be at 300,000 in just 14 seconds
That was also my intuitive response at the beginning of the pandemic. I assume one virus was plenty due to exponential growth. Having read every article I could in the past year, it's extremely rare to run across any details but:
1. I've read that scientists believe a coronavirus takes hundreds of viruses to successfully infect us. Not, for example, several dozen like some other viruses.
2. Next obvious question to me is, is this because one has to land on a lucky spot on the body and the rest somehow die before they can reproduce (so it's statistical odds that one virus gets the conditions it needs just like one sperm makes it to the egg)? Or can the body fight off a dozen or two dozen covid19 viruses so quickly that they never take hold? I only see two possibilities here.
3. If it is the latter, an answer I can't find anywhere, why did we need to waste so much time developing a vaccine? Wouldn't it be equally efficacious to introduce one virus to the body on day one, four on day two, and so on until immunity is achieved? Evidence of this possibility would be mixed in with the population they believe are asymptomatic, so unless researchers look for this they won't find it. (Basically a natural immunity hypothesis - based on repeated low viral count exposure.)
A virus that doubled in a second would be perceived as a swarm that dissolved people before our eyes as it quickly ate the biomass of the planet. Think 2^86400 in one day. Fortunately it would need faster than light travel to keep replicating at that rate for long.
Anything that keeps replicating exponentially will eventually have its growth limited by the speed of light, because the amount of space you can reach while traveling at a bounded speed only grows polynomially fast. Because the formula for the volume of a sphere is cubic. You’ll run out of space and the things in the inside of the ball won’t have room to replicate.
> If it is the latter, an answer I can't find anywhere, why did we need to waste so much time developing a vaccine? Wouldn't it be equally efficacious to introduce one virus to the body on day one, four on day two, and so on until immunity is achieved?
Introducing the virus like this, you’ve created a live virus vaccine. The work involved in creating and testing such a vaccine isn’t really any less than creating the vaccines we did make. You still have to develop technology to grow the virus and distribute exactly the right quantity. Moreover, the risk of complications is far greater if someone fails to fight off the small viral load infection.
The vaccines such as Moderna only took a week or two to prototype in January 2020. The entire rest of the time was scaling up production and running tests to prove it worked in the population. We could have skipped running the trials and deployed the untested vaccine instead. A lot of lives would have been saved but no way to know that without doing the trials, I suppose.
What you are referring to is the viral load. How much does it take to make you really ill. It matters because your body can fight a few dozen virus cells more readily that it can a few thousand. Sure it can make more antibodies but they take time, time the virus has to replicate, so now you need more antibodies, and yiu aren't exactly sure which ones work.
Sort of. Variolation also involved intentionally inoculating with a naturally occurring less deadly strain. Also, introducing intentional Covid infections in a naive population would likely infect many contacts of the inoculated patients before they got inoculated, which would defeat the purpose.
to your last question—when we develop a vaccine or treatment, it’s about making sure as many people as possible get the minimum degree of protection with the least amount of risk. giving live virus is a tremendous risk, even if you found a way to just give one particle at a time effectively.
Viral reproduction rate is not that fast. It's about 8 to 72 hours depending on the type of virus. This is why low viral load is generally associated with milder disease outcomes, the body has a significantly longer time to generate an immune response before the viral load becomes significant.
It doesn't only react faster, it will react differently. Up to a reaction called "sepsis" that can kill you even without the virus doing anything anymore. Research points to most covid complications being such (there are lots more, the immune system is the worst kind of spaghetti code you can imagine) massive immune reactions gone haywire.
I'm not saying you are right or wrong. I'm saying that immune reactions aren't linear, straightforward, harmless or predictable. And that "more virus" usually isn't better.
As a type1 diabetic, I love the 'spagetticode' reference. Our biology is amazingly complex. And in a somewhat constant broken state. My immune system decided that crucial pieces of my own body, are dangerous invaders, and it then decided to attack it. The attack is ongoing, and successful: a crucial subroutine of me is being destroyed faster than another part of me can rewrite it.
This isn’t really accurate because it fails to take into account how infections work. Viruses don’t replicate like bacteria, so they don’t just double every X amount of time. They infect a cell and hijack the cell to produce copies (sometimes millions) of the virus until the cell exhausts itself and dies, bursting open and releasing all those copies of the virus. While this is happening, the body is attempting to fight this. What is particularly relevant are several of the varieties of T-cells, or killer cells. They are attempting to find cells infected with the virus and destroy them before they burst. While some copies of viruses escape cells as they are producing them, the overwhelming majority escape when it dies and bursts.
What this means is that 30 viral particles do not become 300,000 in 14 seconds. Say that all 30 find cells and infect them, and T-cells destroy 50% before they burst. You have 15 cells that burst and release viruses to infect nearby cells. If you start with 300,000 infected cells, and T-cells destroy 50% before they burst, you have 150,000 cells that burst and release viruses to infect nearby cells.
Low initial infections can often be well controlled and managed by the immune system in this way until antibodies are produced. High load infections can often spiral out of control due to so many initial cells being infected, the physical damage of higher numbers of killed cells, either burst or destroyed, and the high numbers outpacing the body’s ability. Of course this is also a simplification, but I think it demonstrates how initial viral load can have a big effect on outcome.
Won't the immune system acts better when it gets infected by 30 (say) virus particles than swamped by 300k viruses (say).So my guess (as layman) is when infected with 30 viruses the growth might not be as uncontrollable (doubling per second). I think the virus load indeed matters too.
You are right, but in the early phase of the pandemic this was raised by medics in the UK as a reason why some of them were dying. The pathology mentioned then was that a cytokine storm got kicked off in people with strong immune systems exposed to high load. This prompted changes in PPE for hospital staff - from light gear that would be worn in the face of flu patients (of whom, as we know some 1000's are hospitalised and die every year) to the space suit style gear that is now used in ICUs with COVID. If you are young and nursing a bunch of relatives at home it's reasonable to say that you are effectively exposed to ICU risks without ICU gear.
I work in an ICU. Bedside staff is equipped with PPE2. No space suit. I've spent months of my life wearing only a surgical mask in what is basically a COVID aquarium, with patients on non-invasive ventilation in open-space units spraying virus everywhere. Our staff case count of hospital-acquired infection is currently zero. So, I don't know what the ground truth is but it certainly seems like exposure is not the only factor.
So - that's amazing to me. In the beginning of the pandemic the stats seemed to show that hospital staff were at significant risk. I think that this has faded from the numbers in the UK and my assumption was that this was because staff were now able to protect themselves with good PPE and vaccination.
If you're young the first is probably a mild cold while the latter is a trip to the ICU.
Part of bringing the virus under control is reducing the amount of particles people are exposed to so they have a better chance of fighting off the virus.