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Comment by cm2187 | Hacker News Reader

It does, the more young healthy people are immune, the less likely the virus will make it to them.

Being asymptomatic is not the same as being immune. It means that more people will feel fine and spread the virus more because they don't know they have it.

Well, for what it's worth, if they get the virus while on a long tour of duty, by the time they get back they should be good to contribute to the herd immunity.

Only if they form antibodies. Studies have been suggesting that people who get it in asymptomatic form are not all forming antibodies - leaving them wide open to be future communicators of the disease.

There are no studies that have suggested anything like this. There simply has not been sufficient time to perform a study of the type needed to prove such a claim: you would need to gather a cohort of people that you know had the virus, wait for them to recover, then test for antibodies.

Moreover, even if the percentage of such people were shockingly high (i.e. over a fraction of a percentage), you would need to conduct a huge survey to distinguish it from error rates on the tests themselves.

That sounds really interesting, could you please link to more info about this?

I'll check back in here later with links - didn't save it at the time I was reading through.

To everyone suddenly thinking about antibodies vs T-cells vs whatever else, the podcast "This Week In Virology" discusses some of the difficulties at https://www.microbe.tv/twiv/twiv-602/ (discussion with Stanley Perlman). A number of other episodes also hit on coronavirus. Listen while you're walking the dog.

Another fun seminar is this one by Prof Pamela Bjorkman at Caltech; it's useful to watch the slides with at least one eyeball so not for dog-walking. https://www.youtube.com/watch?v=OBcc_dk9Q9U

Forming antibodies (antibody driven adaptive immunity) seems like the most likely way patients are recovering. This would be typical of recovery from Coronavirus infection.

https://www.nature.com/articles/s41591-020-0819-2

I can’t find any research suggesting that patients (symptomatic of not) are recovering in some other way.

And in any case, recovery implies some form of immunity, either innate or adaptive. The virus doesn’t just give up after 14 days.

Or maybe it was a false positive.

Wouldn't that mean that a vaccine is close to impossible?

My layman understanding is that a vaccine relies on the body creating antibodies.

A known failure mode of vaccines is if the person who is being vaccinated lacks the right B cells for creating antibodies matching the antigens on the surface of a pathogen. If the B cells a person has lack the right B Cell receptors, they can't generate the correct antibody response to an antigen, because they can't bind with/identify an antigen in the first place. Additionally, they may lack a sufficient number of antigen naive T cells, which haven't yet become differentiated as T memory cells and effector T cells.

But that doesn't mean that it is impossible to create a vaccine: this problem exists already for successful vaccines. For example, the Hepatitis B vaccine has a relatively high failure rate, but is still provides immunity 90+% of the time. It just means that some smallish percentage of the people you vaccinate aren't actually contributing to population immunity.

See below for more info:

https://en.wikipedia.org/wiki/B_cell

https://en.wikipedia.org/wiki/Memory_B_cell

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3760154/ --> this one is particularly good. A lot of good info in here on how vaccination and "memory" interact.

https://www.sciencedirect.com/science/article/pii/S0264410X0...

EDIT: this one covers the major routes of vaccination failure --> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4962729/#!po=60...

It’s possible and desirable for a vaccine to stimulate antibody production where a “natural” infection would not, which is one of the things that will be tested during their development. An extreme example is infection with the tetanus-causing bacterium clostridium tetani, which doesn’t provide natural immunity at all.

It's not clear to me that asymtomatic doesn't mean immune. If the primary symptoms are due to over-replication of the virus and not fighting it enough resulting in cell death in lungs and other airways, then asymptomatic infection indicates the immune system is fighting it enough to fend it off.

Now, this rests on symptoms being directly caused by higher virus cell counts rather than toxic byproduct cascades of some sort. I'm not sure that's true

This is devolving into semantics. Being a asymptomatic means you are infected, which means you are not immune. You can still develop symptoms later and/or still transmit the disease.

You would be considered immune if your body produced antibodies that prevented infection. This immunity can be gained by successfully fighting the infection or by receiving a vaccination that triggers an immune response.

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