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A Nobel prize winner explains coronavirus

Apr 2, 2020 • 16m 15s

Professor Peter Doherty won the Nobel prize for his research on how our bodies fight off viruses. Today, we ask him what makes Covid-19 different from other infections, and what we should be doing now to prepare for the next pandemic.

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A Nobel prize winner explains coronavirus

195 • Apr 2, 2020

A Nobel prize winner explains coronavirus

PETER:

Hello.

RUBY:

Oh, hi, is this Peter?

PETER:

Yeah. Yeah.

RUBY:

Hello. Hello. It's Ruby Jones from Schwartz Media.

PETER:

OK. Are you hearing me OK?

RUBY:

I can hear you okay. Can you hear me okay?

PETER:

Ah pretty well. These are pretty crap phones.

RUBY:

Well, it sounds okay at my end. So let's roll with it.

PETER:

Okay, good.

RUBY:

Peter, I was just wondering if you can tell me a bit about yourself and describe what you do for work.

PETER:

I'm Peter Doherty. I'm a professor at the University of Melbourne and patron of the Doherty Institute. I've worked for more than 50 years on immunity to virus infections and particularly focused on the pathogenesis of virus infections, the way viruses cause disease. Now I find myself in the middle of COVID19 and suddenly I'm relevant.


RUBY:

From Schwartz Media, I’m Ruby Jones, this is 7am.

Professor Peter Doherty won the Nobel prize for his research into how our bodies fight off viruses. He wrote about the Covid-19 pandemic for The Saturday Paper.

Today - we ask him what makes Covid-19 different from other infections… and what we should be doing now to prepare for the next pandemic.


RUBY:

Peter, you've been researching and writing about infection and immunity for many decades. Given that, I imagine that you would have understood the severity of COVID19 from fairly early on. Can you tell me about when it became serious for you and when you realized that it could be different?

PETER:

I think as soon as I heard about it, it sounded dangerous. And then, of course, as it built up in Wuhan it looked very, very dangerous. And we all caught on to that fairly quickly. The dangerous part of it for me was that it was spreading so quickly. It kills less people than the old SARS virus. We're calling it SARS1 now that circulated 2002/2003. But it's infinitely more infectious, which makes it much, much more dangerous.

RUBY:

So talk to me about that. How does Covid-19 compare to other viral infections like SARS and MERS?

PETER:

These three viruses are all what are called beta coronaviruses.

We are pretty certain they all come originally from bats that then transmit to some other animal with size one with a little animal called a civet cat. That animal was being sold in live animal markets in southern China and jumped into humans. The size 1 killed about 10 per cent, I think of the people as infected.

Then a few years later, 2012, we suddenly encountered MERS, Middle Eastern Respiratory Syndrome. It's an equivalent disease again. It's a virus we think went from bats to camels and then camels to people. It has about a 30 percent mortality. So it's a really dangerous one.

Then we think COVID19 is caused by what we call the SARS Coronavirus2 COV2. And that we think went from bats maybe to pangolins in a again, a labor or market in Wunan and then to people. And it's killing, well, initially the death rates reported were 2.5 percent from Wuhan. More recently, since they've analyzed background infections. There's a lot of asymptomatic or very mild infections with this virus. It's down to 1.4 per cent for this series.

RUBY:

And there are also reports of different mortality rates for Covid-19 in different countries. Why is that… and just how deadly is Covid-19?

PETER:

Yes, the issue of mortality rates it's related to how many people you're diagnosing as positive. So what we have testing for is the presence of infectious virus and that's all we've been testing for.

Now, what we need beyond that is what's called an antibody test. So once people are antibody positive, then we can tell whether they've had the infection. And we need to use that test because a large number of people have very mild infection or even inapparent infection - they may not know they've had anything at all. So we need to screen large numbers of people for the presence of antibodies.

Now, that's why that's important is we need to know how many people are and have been infected. If we have a clear statement of mortality rates. So in Spain and Italy, I have the impression that they're only really testing people who show up with signs of sickness. So that will give you a very high mortality rate because they will be the ones that consensually go on to develop disease.

So that's why in Wuhan, the initial mortality rate was 2.5 percent. But they went ahead and did a lot more testing and they were testing the virus not for antibody, they've reduced that 1.4 percent. So if you then went ahead and you test all those people for antibody, you mind might find it's much lower than that again.

RUBY:

And Peter, what does COVID19, do to the body that makes it so dangerous?

PETER:

Well, basically, it grows initially in the upper respiratory tract. Then it gets down into the lung. Now, if it stays in the upper respiratory tract, we're fine. We might just experience symptoms of a cold. You may have headaches and that sort of stuff, but you won't be too bad.

Now, the problem is when it gets deep in the lung, firstly, the virus is doing some damage because it can kill cells, but it's also the host response that's trying to get rid of it, that brings in all sorts of rather toxic molecules which can cause blood vessels to leak. We get edema and we get inflammation. And what happens then is that the bronchioles in the lung will wear red blood cells, bring carbon dioxide and exchange that for oxygen, get clogged. And if we can't get enough oxygen, it's very simple. We die.

So that's why people who do get clinically ill, if they're sick enough, will be taken into hospital. Many of those will be handled in wards where they're simply given more oxygen or given a bit of help in breathing and stuff. But you actually have to be intubated. You have to ever to put your trachea. Then you're probably in pretty bad shape. The lung is such a delicate organ and it's easily compromised.

RUBY:

Covid-19 isn’t the first viral pandemic we’ve experienced. Back in 2009 37,000 Australians contracted swine flu, and 190 of them died. What’s the difference between the way swine flu spread and what we’re experiencing now?

PETER:

Well, swine flu was a classic pandemic influenza A virus. And in this case two different pig strains somehow got together and we got a new virus out, which was extremely infectious for humans.

This went round the world very, very quickly. We were all terrified initially because we thought this might be a repeat of the terrible 1918/19 flu pandemic which killed 50 to 100 million people.

The H1N1 swine flu virus wasn't terribly severe. In fact, it was no more severe than what we call the normal seasonal influenzas.

And the reason wasn't so severe is that people who were around and around in 1977 seem to have been infected with a somewhat similar virus which gave them cross protection. So older people didn't die from me from the H1N1 swine flu. They’re normally the people who are most susceptible. We did get a number of very severe clinical cases and deaths in young adults, including heavily pregnant women. It also was rather bad in indigenous societies, but that's always true of these viruses.

RUBY:

So some people were actually immune to swine flu. Is there any immunity to COVID-19?

PETER:

No, we had no no preexisting immunity to COVID19. It's what we call a virgin soil pandemic.

RUBY:

We’ll be back in a moment.

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RUBY:

Peter, we’re talking about the ways in which Covid-19 is different to pandemics we’ve seen before. Are there any other recent examples of what you called a ‘virgin soil pandemic’ - where we have no pre-existing immunity?

PETER:

The latest example of that we're all familiar with is Zika virus. When it got into South America, it had been circulating around in the Pacific for some considerable time and most of us heard nothing about it. But then we heard a lot about it because it was causing fetal abnormality. But we did nothing about it now. And that's because in South America, they presumably developed herd immunity to this virus. They never used a vaccine. It's just a lot of people must have been attacked and most of them were infected without any severe consequence, of course.

RUBY:

Can you explain the concept of herd immunity to me and why it doesn't rely on a vaccine?

PETER:

Yes, it's pretty simple, really. The more people get infected and recover, the more people are immune. Once they've recovered and they’re no longer pushing out virus, the less virus there is around the place.

So at a certain point, depending on the transmissibility of the virus, you achieve what's called herd immunity. When the case loads with new cases it will suddenly drop dramatically because there's not that many people to infect anymore and there're many less people to transmit.

Now, with many viruses, we reach that herd immunity at about 50 to 60 percent of the population being infected. Measles need about 85 to 90 percent of the population immune before we get herd immunity. So we're hoping that it will be down around the 50 to 60 percent level for COVID19.

Now, of course, the issue there is that if we're successful with our sequestrations and decreasing social contact and so forth in slowing the spread of this virus, it will take much longer to get to that herd immunity level. So the longer it takes to get to that level, the longer the economic damage. So what's being suggested, that moment it's coming out of Britain, but I've been suggesting it here is they've put it rather nicely that we should have immunity passports, that people who have been infected probably not going to get infected again, should be given a passport saying that's the case and then they could return to work. So that's great. But then that creates a lot of social and psychological problems.

So it's a very complex issue. This whole thing that's a mixture of the hard science of infection and immunity, psychological science and of course, political realities. And that's why people like me are great at talking about the hard science. But it has to go further up the tree with a lot more input from different sorts of people as you determine policy.

RUBY:

Mmm so bearing that in mind, what do you think we should do to prepare for the next time one of these viruses makes the jump to humans?

PETER:

Well, we should do a number of things, and that's a long term strategy discussion that'll go on after this. And I think there's been a big wakeup call. I think we'll get better.

Some things were being done to prepare. There was an international organization that was funding vaccine research for newly emerging pathogens.

The thing we missed is we could have been developing class specific anti-coronavirus drugs.

And we had those for influenza. Drugs like Tamiflu and Relenza and so forth, work against all the influenza viruses. And we could have had drugs that work against all the coronaviruses.

So I think that's one thing we might do as we go forward is after we're through this look at all the types of viruses that could potentially infect us and develop drugs that could limit the growth of those viruses.

RUBY:

Hey Peter, just before we let you go - the producer here wanted me to ask if you’ve seen the film Contagion?

PETER:

Oh yeah course. I know the guy who was the medical advisor on it. You know, it's the one time that Hollywood has actually taken notice of the medical professional, you know, other than other movies about this sort of stuff, like outbreak, are total crap. But no, it’s a good movie.

RUBY:

Peter, thanks so much for talking to me today. I feel like I’ve learnt so much.

PETER:

Okay. It’s a pleasure.

RUBY:

And the latest in the response to Covid-19:

Australia’s Deputy chief medical officer Paul Kelly yesterday said that while the amount of Covid-19 cases continues to rise, the curve is flattening.

Kelly said that while that’s good news... it is not time to take the foot off the brake. He also urged Australians, especially those aged over 65, to get their flu vaccines as soon as possible.

Minutes from the Reserve Bank’s last meeting reveal fears that the economic fallout from the pandemic could last over a year. However, the RBA did rule out negative interest rates as a strategy to address the downturn.
_

In Victoria, the state government has announced it will boost the number of intensive care beds nearly tenfold to bolster the state's capacity to deal with the COVID-19 pandemic. The 1.3 billion dollar funding boost will be used to expand the number of intensive care beds from 500 to 4,500.
_

Over 4800 cases of COVID-19 have been confirmed in Australia and 20 people have died since the beginning of the outbreak.

Globally, coronavirus cases have exceeded 850,000, according to the Johns Hopkins University tally. As of yesterday afternoon, more than 42,000 people had died.

Description: Professor Peter Doherty won the Nobel prize for his research on how our bodies fight off viruses. Today, we ask him what makes Covid-19 different from other infections, how it damages our bodies, and what we should be doing now to prepare for the next pandemic.

Guest: Professor Peter Doherty.

Background reading:

The pandemic we had to have in The Saturday Paper
The Saturday Paper
The Monthly

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7am is a daily show from The Monthly and The Saturday Paper. It’s produced by Ruby Schwartz, Atticus Bastow, and Michelle Macklem. Elle Marsh is our features and field producer, in a position supported by the Judith Neilson Institute for Journalism and Ideas. Brian Campeau mixes the show. Our editor is Osman Faruqi. Erik Jensen is our editor-in-chief. Our theme music is by Ned Beckley and Josh Hogan of Envelope Audio.

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195: A Nobel prize winner explains coronavirus