UKC

If you've had Covid then presumably you've got some level of immunity for some period of time, but as time goes on the working assumption is that the amount of immunity will decrease.

So if you come into contact with Covid again, you will still get the virus in your body but your immune system should react more quickly and the viral levels should (hopefully) never build up to a harmful amount.

Will this 2nd contact with Covid act like a vaccine booster shot - in that the immune system gets a 2nd go at producing the necessary antibodies etc - so presumably that should strengthen and lengthen the amount of immunity you have.

And if that's correct, should people who've had Covid (and are fully recovered) be trying to get a re-exposure at low levels to strengthen their immune response? (Edit: I'm not actually suggesting this but to me it does seem to logically follow on)

Thoughts please as to whether this line of reasoning is flawed or whether it makes sense.

In reply to Michael Hood:

Yes, in principle your second exposure should produce a faster and stronger ‘anamnestic response’, although generally being exposed to to real infection would be enough to generate a pretty good level of immunity sufficient to prevent clinical symptoms the second time.  Vaccination often  isn’t quite as good at this, hence the second shot.

That said, common cold-type coronaviruses don’t seem to be very good at generating long-term protective immunity, so who knows how this will play out for SARS-CoV-2.  It seems that the worse you get COVID-19 the better your immune response and I would guess that any subsequent infections would be less serious, but there’s a lot we still don’t know about long-term issues.

In reply to Michael Hood:

from reading a couple of articles about people who have had a second infection from a different strain the jury is out - one had it mild the second time, the other was hospitalised.

In reply to Michael Hood:

Risky but only on the basis of one news report.

https://m.jpost.com/israel-news/israelis-who-fell-sick-with-covid-19-twice-...

I an unsure if there is a scientific consensus.

In reply to Michael Hood: some thoughts - one could answer with a Rumsfeld 'there are knowns...'

1. Yes there should be a faster response. Memory T-cells will initiate cellular and antibody responses, which previously had to slowly develop. However there is some doubt how long these last. Antibodies may fall quickly and in previous SARS the virus has been shown to inhibit antibody production to some extent.

2. Repeated re-exposure of the virus to immunocompetent people (through previous exposure or vaccination) will lead to increased selection pressure on the virus to change defeating immunity a little or a lot (shift and drift). 

3. The induction of profound immune responses in reinfected immunised / exposed people has led to more severe signs in some diseases (e.g. Dengue) and COVID19 may be one of these. The 'cytokine storm' that results leads to more severe disease due to an inappropriate immunity.

In reply to SouthernSteve:

Thanks, those are the kind of "stumbling blocks" I was wondering about.

This is all coming from me realising that just because I've had it once, doesn't mean I won't have the virus in me if I come into contact with it again - it's not like the virus says "he's had it already, let's not go there".

Just (hopefully) means that any viral levels I would have would be lower. And hopefully would mean that my viral levels would be low enough so that I'd be unlikely to transmit to others (elderly parents).

Too many unquantifiable unknowns ☹️

In reply to Dave Garnett:

There are over 200 viruses that cause the common cold. There’s only one SARS-COV-2 virus. Or possibly two depending on your view and an isolated case of reinfection). 

In reply to DancingOnRock:

Something tells me DG knows that. 

In reply to DancingOnRock:

Yes, but I was referring to the four other known coronaviruses that commonly cause mild cold-like symptoms (229E, NL63, OC43 and HKU1).

In reply to SouthernSteve:

Yes, there are unusual situations where the normal system doesn't work as intended.  There's something called antibody-dependent enhancement where cells of the immune system that are designed to latch onto antibodies that have already identified a target to attack (they have Fc receptors that bind the opposite end of the antibody) are then themselves infected, as happens in Dengue fever (very good article about this here: https://www.nature.com/articles/s41577-020-00410-0).

Antibodies, once bound to their target, have a number of functions.  One is, as just explained, to act as a target for Fc-bearing cells like neutrophils, macrophages and NK cells.  Another is to activate another part of the immune system - the complement cascade, which results in the assembly of a protein complex that can, for instance, punch of hole in a cell membrane and trigger inflammation.  It's complicated (and usually carefully controlled) but occasionally 'non-neutralising' antibodies can do this inappropriately.

Usually, and for most pathogens, all this works pretty well, but what with evolution being what it is, sometimes pathogens arise where it all goes a bit wrong... 

In reply to elsewhere:

This would be worrying if it's much more than a one-off.  All sorts of other things that might have caused this in an isolated case.

In reply to Dave Garnett:

Thanks! I do have a PhD in immunology.

In reply to Dave Garnett:

False positive test for the first infection, for instance.

In reply to Dave Garnett:

Do they circulate regularly? How often they circulate and infect large numbers of people presumably would give an indication.

In reply to Michael Hood:

It might simply damage more of you body than it did the first time, for all we know.

In reply to SouthernSteve:

Sorry!  Didn’t mean to be patronising and I should probably have responded to a different post.  It’s complicated stuff though and there’s an unusually engaged and smart lay audience here as well quite a few experts like you!

In reply to Dave Garnett:

Sorry back, a lot going on here – should have bitten my tongue. 

In reply to...

Guys, it's always useful for us simpletons to know when people have some professional expertise in an area (rather than just - and I'm not meaning this as any kind of belittlement - being a well informed layman - of which there are many on UKC).

Then if you're talking rubbish, at least we'll know it's well informed rubbish 😁

In reply to Michael Hood:

I'm always capable of talking rubbish, and I moved out of professional immunology (I'm shocked to realise) 20 years ago, which is an eternity in a fast-moving field like this.  I do need to keep in touch with biotech generally for my current job though. 

In reply to DancingOnRock:

These viruses circulate all the time because immunity does not last long enough to achieve full herd immunity over several cold seasons. The reason for this is that coronaviruses are rather good at suppressing long term immunity, suggesting that immunity induced by vaccination should work better). This is different from, say, measles, where before vaccination normal epidemic would flame out once herd immunity was reached in a given population, and would only return from a different reservoir population once enough people had been born that did not have immunity from last time round.

Together they cause about 15% of all colds (there will also be many more asymptomatic infections), while rhinoviruses are responsible for about half of all cases, and adenoviruses and a bunch of other families make up the rest.

The really interesting question is whether OC43 coronavirus (and not some influenza virus) is actually the virus responsible for the 1889 "Russian flu" epidemic, in which case it would be interesting to learn how and over which time scale a deadly pandemic virus evolved into a rather harmless pathogen causing mild, common cold.

As I already posted elsewhere, there is no evidence that SARS2-CoV is getting "weaker" during the current pandemic, any changes in case fatality rates will have different causes (more testing/statistical effects, a different segment of society being hit, the most vulnerable patients already dead from the first wave, better treatment options,....)

CB