Antibody diversity is created through a process called hypervariation. It is basically a random generation process. We then filter out those that recognize markers produced by our own body. So each person's antibody will work differently in recognizing the virus, that is choosing what markers to bind to. Whatever antibody that works will go through a clonal multiplication that causes the B cells that produced the antibodies to replicate, conferring resistance to reinfection. So long as your choice of antibody does not happen to depend on the SNP (a seemingly small chance but we also don't know its function for the virus so hard to say) you will be resistant to both types.

How come folks are saying you can get reinfected tho? Has there ever been a disease that the same strain can reinfect someone? Wouldn’t that imply they’d never recover?

Some diseases have 2 phases (biphasic), so you get sick, recover somewhat, get sick again, often with different symptoms.

I've read in the press that corona virus might be biphasic, which is a big problem for an air-borne transmissable disease. In the jet age, quarantining potentially thousands or millions of passengers becomes expensive and disruptive when there's a week between phases.

Lyme disease is like that. First you get a bullseye rash and flu-like symtoms, it goes away, then later your organs are attacked.

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

That's different than a chronic disease, where you never recover.

Why can’t the memory cells help for the second phase?

Shouldn’t the first phase act as a sort of vaccine?

I wonder if it's possible that the virus can take shelter in cells that are not exposed to the antibodies. Don't herpes viruses do something like that? People get chicken pox as a kid, and later get shingles.

I think there have been a few unverified reports of people catching the virus again. However these might be caused by false negative tests (viral load being lower during the time of testing), then they re-take the test when they have a higher viral load(?) and it comes back positive.

This is purely based on other comments I've read, I personally know nothing about viruses.

The exact same way that people repeatedly catch the common coronavirus year after year. 2019's novel coronavirus is destined to end up being known as the "common cold" or coronavirus with time. All common colds are a coronavirus and newly discovered ones are novel. IOW there is no vaccine in the pipeline because there's never been a vaccine for the common cold.

https://www.who.int/health-topics/coronavirus

> All common colds are a coronavirus and newly discovered ones are novel.

Technically not true - coronaviruses cause 15-30% of common colds. The most common cause of the common cold is rhinovirus (30-80%); coronavirus is next, followed by influenza (10-15%), adenovirus, and then other viruses like RSV. The rest of your comment is fairly likely IMHO, though.

But you’re talking about mutations or other strains. My question is can the exact same virus reinfect a person?

I’d think you’d never clear it to begin with if that was the case.

Just to be clarify, B cells undergo somatic hypermutation while undergoing expansion after antigen recognition. On re-exposure, memory cells will be available to identify existing antigens and re-expand the B cells involved with attacking the viral particles.

Immune system is amazing. It can actually detect different strains of the same virus, even if it has never seen that specific mutation. https://www.sciencedaily.com/releases/2018/04/180430212353.h...

> "After exposure to one strain of virus, these memory cells are then better able to recognise variants of the virus if they encounter them in the future. The immune system learns to protect against a whole group of related viruses, not just the one it experienced."

This is kind of a double edged sword though.

Say the virus mutates so that only 50% of its features are recognizable.

You'd think that the fact that your cells can recognize this is good, and it is to some extent, but, it also prevents new cells from learning about the virus(in efforts to prevent autoimmunity in analogous scenarios with non malicious objects; our immune system has to walk the fine line between being too permissive and allowing infections, and being too restrictive and murdering its own host through nasty autoimmune diseases).

So, it mounts a 50% response, which is often good enough, and more than makes up for the more limited response with speed.

But what happens when the % recognizable drops to like 3%? Some percentage of cells will recognize the 3%, and be able to mount a weak response, but more critically, block other cells from developing new responses. This limited response will slow down a proper response and itself will be likely ineffective.

Its known as "original antigenic sin", if you want to read more.

I hope COVID-19 isn't reading this.

I'm pretty sure covid-19 doesn't read Hacker News.

Not that surprising, since an immune system would be very likely to encounter a slight mutation or "variant" of the virus in the future, after the virus spread through others in the population.

But this obviously isn't the case with seasonal viruses such as influenza or coronavirus.

Unknown at this time. It doesn't follow that a specific mutation would mean that your immune system would fail to recognize a different strain. Antibodies don't work like that - just look at how the smallpox vaccine was done through inoculation with cowpox, a completely different disease. Scientists would need to study a cohort of people with known immunity to one strain of COVID-19 and see if they can get it again with exposure to a different strain.

It's also unknown whether it's possible to develop immunity to COVID-19 at all, with reports of reinfection in both China and Japan.

Maybe I'm misunderstanding something about the immune system, but that doesn't seem possible. How can you eliminate a viral infection without developing immunity to the virus causing it - aren't they both the same underlying process?

if the virus is particularily good at shifting the code that corresponds to Epitopic Regions of its antigens, namely those found on the spike protien of the virus then its in an arms race with the immune system.