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Comment by nostrademons | Hacker News Reader

There's some pretty sharp criticism of this paper on the r/COVID19 subreddit (which is the one where the scientists hang out):

https://www.reddit.com/r/COVID19/comments/fdsltf/about_the_l...

Basically, there are 111 different mutations, not 2, and it's misleading to point to a single point mutation and set that as the arbitrary division point between strains while ignoring the other 110 mutations that have been catalogued. There is currently not enough evidence for the researcher's claims that this particular mutation causes observable differences in the virus's reproduction or virulence characteristics that the other mutations do not.

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Here's the substance of the criticism written up:

http://virological.org/t/response-to-on-the-origin-and-conti...

"An analysis of genetic data from the ongoing COVID-19 outbreak was recently published in the journal National Science Review by Tang et al. (2020). Two of the key claims made by this paper appear to have been reached by misunderstanding and over-interpretation of the SARS-CoV-2 data, with an additional analysis suffering from methodological limitations."

What about whether or not you can "catch it again" once your immune system has beaten one version?

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."

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.

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.

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.

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?

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

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.

> 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.

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.

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.

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.

> which is the one where the scientists hang out

Thanks for that. There are a lot of subreddits popping up and I've been trying to distinguish between the legit ones and the cryptoprepper ones.

If there are 111 different mutations, does that mean that a common vaccine is highly improbable/impossible?

Not at all.

The effectiveness of a vaccine is related to the effectiveness of the bodies immune response to the virus.

As long as different mutations do not affect the effectiveness of a given immune response provided for by a vaccine, that vaccine will be effective against those mutations.

Mutations can affect many aspects of a disease, and often this means a different level of effectiveness of an immune response, but it really does depend on the specific mutation.

For now, there are no selection pressures on different strains from vaccines; it will be interesting to see what mutations become prevalent once testing of vaccines starts.

Why does it take so long to develop a deactivated vaccine version of the virus to teach our immune system what to attack?

Safety. You have to understand what 'deactivated' means for this virus, and that people won't get significantly sick if you feed it to them. That takes time.

While this is not exactly a direct answer to your question, these pages may be helpful:

https://shotofprevention.com/2018/03/14/how-flu-strains-are-...

https://www.cdc.gov/flu/about/viruses/change.htm

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