Covid 2023

[malcolm]

Not wishing to make light of something that may affect some seriously, but my wife and I have both just caught Covid for the first time.
Both well into our seventies, and I have a lung condition.
2 years ago, this would have been a potential death sentence, especially for me.
Now, it's just "that's annoying, I've got Covid and feel a bit rubbish"
Temperature 101.6, snotty nose, feel tired, but otherwise all ok.
We've had 4 jabs to date which must help, but it's funny how all viruses mutate overtime so they don't kill the hosts. Look at the flu - no vaccination until comparatively recently, but it still went from a killer to just another damn virus.
Still feel like shit though!

[Series1 Stu]

That's bad news, Malcolm.

I brought Covid home after a visit to the office on 4th December and found myself confined to bed or the sofa for a couple of weeks. I, of course, shared it with my wife and it was the first encounter for both of us. Neither of us tested negative until 23rd December.

I was back to strength fairly quickly after testing negative but, unfortunately, my wife seems to be suffering Long Covid and has very little energy. Previously, she could spend 10 or 12 hours in the garden without complaint but now 2 hours is more than she can manage. Fortunately, she works from home but is supposed to go into the office once a week, which is something she can't manage due to the 80 minute drive each way.

I hope neither of you suffer the same fate.

You are right, 4 jabs has probably ensured we didn't suffer as badly as we might have. I understand they are going to roll out a 5th jab for the over 70's so you should get another go.

Let's hope you get better soon.

Good health!

[RICHOT]

Hope both of you get well very soon so that you can get out and enjoy driving your Jag.

[abowie]

but it's funny how all viruses mutate overtime so they don't kill the hosts.

That's exactly what coronaviruses do.

If you consider the best way for a virus to continue to survive, it needs to be able to spread itself effectively throughout a host population, and maintain that over time.

The best scenario is a virus that is very infectious (high R number) and easily passed on to another host.

But if you kill your host (eg Ebola with 50 to 70% mortality) the infection quickly burns out. Not good for the virus long term.

Similarly you want your host to be able interact with as many other potential hosts as possible. So a relatively mild disease with, ideally, a lot of shedding of virus over the longest period possible. You're a bit sick, with a runny nose and a cough but you still go to work and soldier your way around Sainsbury's.

The final thing the virus wants is to be able to reinfect the same host again later. So it needs to change its immune signature enough that the host still catches the disease next time. Coronaviruses' strategy is constant mutation.

The problem with mutation is that while it has many benefits it also has a downside, which is alterations in the pathogenicity, infectiveness or other effects on the host. So every now and then there's a mutation that produces unexpected effects in infected hosts.

The initial strains of Covid in 2019 had mutated in a way that made them much more pathogenic than the usual coronavirus, resulting in a 1% death rate.

The whole pandemic thing is quite interesting.

Coronaviruses (aka the common cold) are endemic in our population and always have been. Everyone gets a cold every now and then. And we keep getting them because it mutates. Prior to Covid, despite a fair bit of effort, no one successfully produced a vaccination against the common cold, as much as anything because of the coronaviruses' immune mutagenicity.

So logically, all of this has happened before, from time to time. Every (decades/century?) a coronavirus emerges with a bad mutation that kills lots of people.

So what was different in 2019? One major thing. PCR.

In 1995 I did a stint of my anaesthetic training in ICU. This is a requirement. That winter we had an unusually high number of ICU admissions and deaths due to what we called "atypical pneumonia". We assumed it was viral, antibiotics made no difference, we had no effective antivirals at all and we never worked out what the causative virus was.

Back then the only way to ID the pathogen was to measure patient antibody titres. These take days or weeks to rise after infection and if the patient dies within 48 hours you can't ever measure them.

And I only saw the patients who were presented for ICU admission. The frail elderly in nursing homes mostly never even made it to hospital, never mind being considered as ICU candidates.

But roll on to 2019 and suddenly you had PCR and this was an absolute game changer. You could know what the infectious agent was within 24 hours.

The ability to identify Covid infection enabled public health strategies to minimise the spread of the virus (lockdown and isolation), development of effective antiviral medication (previously undreamed of) and to produce an effective vaccine.

So in 1995 we looked back after winter a bit nonplussed and felt that it had been an unusually bad time, but had absolutely no idea what had caused it and didn't even know how many people had died.

Roll on to now, and with PCR the causative agent is right there in the spotlight.

[abowie]

And at the risk of really boring you, a bit more about PCR.

Polymerase Chain Reaction is a way to sample tiny amounts of nucleic acid (DNA) and duplicate the DNA by many orders of magnitude. This leaves you with a sample with enough DNA in it to positively identify it, and thence the organism it came from.

You can take a sample of river water, run it through PCR and identify the DNA of every thing that lives in that river.

PCR uses an enzyme called Taq polymerase. Taq polymerase is nothing short of astonishing.

DNA is a double strand of strings of chemical building blocks called bases. Each base on one strand corresponds to a matching base on the other string. So you have two corresponding strands zipped together.

A piece of DNA is basically an instruction for the manufacture of a protein. Like the punched paper roll on a pianola. In order for the DNA to do it's thing it has to be unzipped to a single strand and then fed into enzymes within the cell that read the DNA and churn out the product.

In the PCR reaction once each strand of DNA has been copied by the Taq polymerase you end up with zipped up double strands.

But in order to copy the DNA again (and again and again; usually 30 plus times) it needs to be unzipped. The best way to do this is denature it using heat. The problem is you need about 95C to denature the DNA, but most enzymes get destroyed above 55C.

Unless your enzyme comes from a bacterium that lives in deep sea volcanic vents and copes perfectly well with boiling water. Which is where our Taq (Thermus aquaticus) polymerase enzyme comes from.

Which I find simply mindboggling. Taq has been quietly existing for hundreds of millions of years just so we can have PCR.

[malcolm]

Thanks Andrew, very interesting