Professor Sunetra Gupta provides a wise, wholistic perspective on the pandemic in her interview published at Reason We may already have herd immunity. Excerpts in italics with my bolds. H/T Paul Yowell.
I particularly appreciate her sense of the complexity of multiple factors and values, and humility in the challenge of getting the balance right. This contrasts with so many narrow and overly confident technical pronouncements we read and hear in the media.
Are we already immune to coronavirus? Professor Sunetra Gupta, a theoretical epidemiologist at Oxford University, discusses her recent study on the herd immunity threshold, as well as her views on the social costs of lockdown, the inaccuracy of epidemiological models, and the curtailment of academic debate.
A study produced by a team at Oxford University indicated that some parts of the United Kingdom may already have reached herd immunity from coronavirus. A significant fraction of the population, according to the study published last week, may have “innate resistance or cross-protection from exposure to seasonal coronaviruses”, making the proportion vulnerable to coronavirus infection much smaller than previously thought.
The Oxford team is led by Sunetra Gupta, a professor of theoretical epidemiology. In recent months, she has argued that the cost of lockdown will be too high for the poorest in society and questioned the language and quality of debate on the pandemic’s impact.
Reaction interviewed Professor Gupta about these matters and more, with questions from Maggie Pagano, Alastair Benn and Mutaz Ahmed.
Yes, exactly. The principle of protection from exposure to related viruses, and indeed any kind of pathogen, is one that we’ve known for a very long time. The very first vaccine we had, which is smallpox, was based on the idea that cowpox protects against smallpox. This idea was already there well in advance of us knowing that smallpox was a virus – and indeed in advance of germ theory having been properly established. So we knew about this cross protection even before we knew that diseases were caused by germs. It’s a very old idea.
In my own studies, beginning with malaria and then later thinking about flu, the role of cross-immunity in protecting against disease seemed to be something that very much needed to be factored into our thinking. Most of the people who die from malaria are children, and they die upon their first exposure, because they have no immunity at that stage. That was one of the first things that struck me when I was working on malaria.
And then later when I was working on flu, it seemed to me a very good way of explaining why the 1918 flu had killed so many people, but why that didn’t seem to be repeating itself, was that it was likely that people hadn’t been exposed to flu. Many people would have not had the flu at all. So then that built up this population of naive immunity in people under the age of thirty who were very badly affected when the pandemic came through.
Having those ideas in mind, when the Covid-19 virus started to spread, I was pretty certain it wouldn’t have a huge, devastating impact in terms of mortality, because we had all these other coronaviruses circulating.
What I didn’t anticipate was that some of our responses to previous exposure to seasonal coronaviruses might actually protect us from infection. It’s one thing to get infected and not ill, but what the new studies are showing is that people are actually fighting off infection. So at an even more basic level, the pre-existing antibodies or T-cell responses against coronaviruses seem to protect against infection, not just the outcome of infection.
Low Seroprevalence May be a Good Thing
What we know is that the seropositivity rates in many parts of the world are much lower than we’d expect them to be if we assume that the epidemic has passed through and that people are resistant. If you take a very simple scenario where everyone is susceptible, you’d expect 60-70% of them to have some marker of exposure. And that is not what’s been observed.
One of the things that’s been done in reporting the seroprevalence, which is not correct, is that they’ve been homogenised. When people say only 5-6% of the UK population has been exposed, that’s not correct. I think very few people would agree that exposure rates in London are less than 20%.
The picture that we’re getting is heterogeneous. But even in hotspots, apart from a few reports, they’re still quite low. So why is that?
One reason might be that lockdown stopped the spread of infection, so it was halted at a stage when, say, 20% of people were immune and the rest of the people were still susceptible to infection. Well, under those circumstances, the easing of lockdown should result in fairly rapid growth of cases. And that’s not something we’re seeing.
So we’ve got those two bits of information. The third bit, the missing piece of the puzzle, is this idea that some people are fully resistant to infection, because they just have really good defences. That could just be part of our innate immunological makeup. It’s also becoming clear that some of the people that have beaten it off have had responses to other coronaviruses which could have played a role.
The other bit of the puzzle is that some people do get infected and they make antibody responses, but those responses die very quickly. So if you’re trying to measure exposure, you won’t get the full picture. Some of the measures of seroprevalence might be underestimates.
We’ve got four pieces of the puzzle, then. If we put them all together, which is what the paper that we published on Friday does, it gives you a theoretical framework that you can use to look at how these bits connect up together.
You can see two things. You can see why the seroprevalence level might be low, and you can also infer that the level of herd immunity needed to stop the thing from exploding again is actually much lower than the figures that are currently being thrown around quite incautiously might suggest.
The fifth piece of this jigsaw could be that there is some seasonality. I suspect that in the winter it will probably come back, but hopefully only to the regions where it was kept from going by lockdown, and where the seroprevalence levels are genuinely extremely low.
We can be cautiously hopeful that in areas where the seroprevalence levels have achieved a certain value that’s compatible with there being a proportion who are resistant, that it might not come back with such vehemence.
Quality of Life Matters
What’s disappointed me about the way this has been approached is it has been approached along a single axis, which, if you like, is a scientific one. Even within that context, you could argue that it’s too one-dimensional, so we’re not thinking about what’s happening with other infectious diseases or how many people are going to die of cancer.
That’s the axis of disease, but then there’s the socioeconomic axis, which has been ignored. But there’s a third, aesthetic access, which is about how we want to live our lives. We are closing ourselves off not just to the disease, but to other aspects of being human.
I think the trade-off is very extreme. Obviously the most extreme manifestation of that trade-off is the 23 million people who will be pushed below the poverty line as a result of this sledgehammer approach. The costs to the arts is I think also incredibly profound – the theatres and all other forms of performing art. But also the inherent art of living, which I think is being compromised.
Acts of kindness are being eschewed. Someone was telling me yesterday that their mother said to them “please don’t come home, you’re going to kill us”.
Carrying On with Living is Social Responsibility
Because actually, the only way we can reduce the risk to the vulnerable people in the population is, for those of us who are able to acquire herd immunity, to do that.
Even if there is a little bit of a risk. I’m 55 years old, there’s some slight risk out there. But I would be willing to take that, just as I do with the flu. There’s a risk I might die of flu, but I’m willing to take that risk, because I know that if I don’t then flu will appear as it did before, it will enter the population of immunologically naive individuals, and then there will be a high risk of infection which will have a disproportionate effect on the vulnerable sector of the population.
Maybe the way to counter it now is to say, actually, not only is it a good thing for young people to go out there and become immune, but that is almost their duty. It’s a way of living with this virus. It’s how we live with other viruses. Flu is clearly a very dangerous virus, but the reason we don’t see more deaths from flu every year is because, through herd immunity, the levels of infection are kept to as low a level as we can get.
The truth is that herd immunity is a way of preventing vulnerable people from dying. It is achieved at the expense of some people dying, and we can stop that by preventing the vulnerable class in the process. In an ideal situation, you would protect the vulnerable as best you can, let people go about their business, allow herd immunity to build up, make sure the economy doesn’t crash, make sure the arts are preserved, and make sure qualities of kindness and tolerance remain in place.
We live, it seems, in this state of terror. Yes, international travel facilitates the entrance of contagion, but what it also does is it brings immunity.
Good Thing It’s Not Our First Coronavirus
If coronavirus had arrived in a setting where we had no coronavirus exposure before, we might be much worse off. It also seems that in addition to protection against severe disease as a result of exposure to related coronaviruses, some fraction of us seem to be resistant to infection.
That’s just fantastic news, actually. Hopefully that will be consolidated at a scientific, laboratory level. We ourselves are looking at how antibodies to seasonal coronaviruses can impact on protection against infection and disease.
Maybe we will be able to build up a picture that will reassure the public that actually we are much better off having been exposed to related coronaviruses. We are in a better place to fight off this infection than we actually thought.
It is widely believed that the herd immunity threshold (HIT) required to prevent a resurgence of SARS-CoV-2 is in excess of 50% for any epidemiological setting. Here, we demonstrate that HIT may be greatly reduced if a fraction of the population is unable to transmit the virus due to innate resistance or cross-protection from exposure to seasonal coronaviruses. The drop in HIT is proportional to the fraction of the population resistant only when that fraction is effectively segregated from the general population; however, when mixing is random, the drop in HIT is more precipitous. Significant reductions in expected mortality can also be observed in settings where a fraction of the population is resistant to infection. These results help to explain the large degree of regional variation observed in seroprevalence and cumulative deaths and suggest that sufficient herd-immunity may already be in place to substantially mitigate a potential second wave.