“…unlike bacterium – in the main – and fungi, they don’t get inside cells. They’re rather large. Some of them are much bigger than the cells, so they can’t be in the cells, they’re in the tissue but in the spaces between the cells and so things like antibodies if you were to make them, that’s where they would joust and do battle and hopefully overwhelm the invader.
But viruses are tiny. Even big viruses like SARS-CoV-2 are small – they easily get inside your cells. That’s what they want to do because they hijack the cellular replication apparatus and force the cell at gunpoint to make billions of millions of copies of themselves. So once it’s inside the cell, antibodies cannot touch it.
Antibodies might be important in slightly preventing internal transmission of the virus from cell to cell inside your body. I’m not convinced that it’s very important. A friend of mine said he’s studied people who don’t make antibodies because they have a problem with their B-cells and they survive respiratory viruses just as well as you and me.
They have bacterial infections all the time but they don’t get problems with respiratory viruses. That tells us it’s not antibodies mostly. It’s T-cells. T-cells, just think of them just think of them as a group of people with special weapons and techniques and they’re all different. They’ve all got slightly different guns and ammo and Swiss army knives and so on.
There are literally tens of billions of variants and it’s just one of the wonders of evolution. When you were made by your mum and your dad there was a shuffle in the region that defines which guns and ammo your T-cells get and you’ve got a whole variety of them.
And the thing is that when a new virus gets into your body, some cells will turn up realize that there’s a wrong one in there and instruct the cell to commit suicide. And they grab bits of the virus and they drag it this bit of the virus into your lymph nodes so it might be in your tonsils or under your arms, in your groin and so on and say ‘oy, I’ve just caught this person invading and causing some smashing, causing some damage’.
And what happens is that virus gets chopped up and the body examines it closely and it presents these little bits of the invader, it’s been chopped up to bits, to your immune system T-cells until one of them goes ‘bloody hell I fit that one perfectly’; and it’s literally by a miracle of natural shuffling there will be several T-cells that fit the invader perfectly and then what they do is some other cells in the system say right you fit the invader perfectly go and multiply. Literally go forth and multiply in a good way, and so you may end up making hundreds of thousands or millions of cells, T-cells that have remembered what you’ve been infected with before.
They just sort of hang around and so if you get infected again you, it will without any compunction and very quickly handle the infection. Now the last thing is if you don’t manage to kill off virus-infected cells with T-cells or natural killer cells or innate immunity and so on, your last ditch stand – it’s like Custer’s Last Stand – you have to get into the process of right we’re going to have to really pull out the big guns and that involves making antibodies and you need another set of cells and it takes a long time. It takes between a week and two weeks, maybe even longer and so you can see that anyone who was symptomatic and survived and didn’t have symptoms for very long, they did not eject the virus because they made antibodies.
They ejected the virus because of one of the other reasons and on T-cells the most important thing to tell you about T-cells is if you’ve been infected by a virus that’s got some similarity, doesn’t have to be identical, some of your T-cells would have recognized one of the chopped up bits that’s similar.
So if you imagine cutting up SARS-CoV-2 into, I don’t know 30 pieces, one of those pieces that your body now remembers as part of a bad one and is able to be immune to. If that’s the same piece in another virus you’ll probably be immune to that one too because basically you haven’t encountered SARS-CoV-2 before but you’ve met its cousins and brothers and you’ve beaten them off. And that’s what’s happened.
This is the thing I’m going to tell you that people will think why weren’t we told this. There are as you said earlier, many scores of respiratory viruses that can make you ill. Amongst those are the coronaviridae family. There are four of them that are what’s called endemic in western, probably around the world. Endemic that means they just wander around and they don’t kill very many people, in fact they kill very few people but they cause about one-third of the common cold.
Common cold causing coronaviruses, you can look them up OC43, HKU1, 229E and I forget the other name [NL63] but they exist and we’ve known about them for 55 years. So they would be in I don’t know, textbooks of immunology. Professor Semple has been on the tv a lot recently saying things I know are not true. He can sue me if he would like.
I looked him up because I thought what’s his training and we’ll get back to SAGA in a minute. Virtually none of them are scientists, biologists or medics. Most of them are very clever mathematicians who mean well and have been utterly led astray by people who do know what I’ve just told you but I’ll just have a little deviation.
I’ve been doing a teaching on immunology and I did have a bit of immunological training but most of what I know I’ve learned during my you’ve used it during applied research. So I’ve read a huge amount over the last 35 years. I’m not an expert but I know enough to spot someone who’s not and lying.
So where was I. Yes so this method of carrying uh memory to related viruses like common cold causing coronaviruses, about a third of us have got exposure to them previously, because there are scores, how many colds do you have in our lifetimes? Not that many. So people say oh well we’d all be immune wouldn’t we? No, how many colds have you had in your lifetime? It’s not that many.
Some people get one every six months. My wife hasn’t had a cold since I’ve met her. She’s probably got good innate immunity right, she spots a wrong one and kills them before they get into her immune system. But this is the point, it’s known, it’s not a guess, it’s not an opinion, there have been six research groups that are let’s call it Oxbridge quality so that you know what I’m talking about.
Karolinska Institute, things like that and six independent research groups of the best clinical and cellular immunologists in the world have published as independently six papers on this topic and several of the papers are in the best journals in the world. Peer-reviewed journals, you don’t argue with those not often anyway.
Science and nature top research journals so and what they say James, you asked me the question what they say is between 20 percent and 80 percent of every single population they studied between them, had prior immunity. That is they could take their T-cells at a time when the virus had not arrived, so this is what this was done like in March or April and they put their little their extracted T-cells in some sort of test tubes like a plate and they could then offer it various pieces of various viruses, and they found that 30 percent of them were able to respond incredibly vigorously to SARS-CoV-2 and they’d never seen it.
In case people say well maybe that didn’t actually confer immunity I’d go no that’s how it works. If they had stimulated them say, because they did, with something else that they’d been vaccinated against like measles or something they could get the same style and intensity of response in their cells, so no it is important, that’s how it works. And so groups around the world showed that roughly, probably the middle estimate was 30 percent of the population had prior immunity and then there was a fantastic paper published I think it was in June.
They know who they are, unbelievably clever work, they did what I’ve described the immune system of doing they cut up various viruses and they got cells from people who had not yet – these were blood down blood donating so they’d been stored a long time but they’re still good – they tested the cells by asking whether the T-cells would respond to SARS-CoV-2. Yes they did, and then in a parallel tube of the same person’s cells, they gave them chopped up bits of SARS-CoV-2 and they gave them chopped up bits of common cold causing coronaviruses and you know where this is going now don’t you?
That when they came to the bits that are most similar between common cold causing coronaviruses and SARS-CoV-2, the cells lit up equally to both of those, and so it wasn’t just by some happenstance that 30 percent of the people had prior immunity. This is the reason, this is the mechanism, so when you look at, if you’re looking in my Lockdown Skeptics article October the 16th, and you’ve got to this point of the podcast please go to the one figure in it, maybe there’s two, but the figure of brightly coloured pie charts – which thanks to my daughter – and you’ll see that SAGE tells you that most people are still susceptible.
I’m telling you and I can prove it and I can show you, the scientists and the quality of the work, and and so on, it’s not true, it was never true that 100 percent was susceptible. At worst it was probably 70 percent and you know this is just so important. So look at the right hand pie chart, 30 percent carry prior immunity. There is no argument about it between immunologists, anyone who studied immunology. Anyone who studied immunology under say the most famous immunologist in Britain at the time was a guy called Ivan Roitt. Every undergraduate of my era that studied for biological sciences had their well-funded copy of Roitt’s Essential Immunology. Mine was like version six, he’s retired he’s still alive well done mate fantastic he’s a colossus of science.”
Source: ‘The Delingpod: The James Delingpole Podcast’ (Oct 22, 2020), https://delingpole.podbean.com/e/dr-mike-yeadon/ (Fair Use)