Achieving COVID-19 herd immunity through infection is dangerous, deadly and might not even work



Under relaxed public health restrictions, deaths will spike far before herd immunity is achieved.
AP Photo/Mark Lennihan

Steven Albert, University of Pittsburgh

White House advisers have made the case recently for a “natural” approach to herd immunity as a way to reduce the need for public health measures to control the SARS-CoV-2 pandemic while still keeping people safe. This idea is summed up in something called the Great Barrington Declaration, a proposal put out by the American Institute for Economic Research, a libertarian think tank.

The basic idea behind this proposal is to let low-risk people in the U.S. socialize and naturally become infected with the coronavirus, while vulnerable people would maintain social distancing and continue to shelter in place. Proponents of this strategy claim so-called “natural herd immunity” will emerge and minimize harm from SARS-CoV-2 while protecting the economy.

Another way to get to herd immunity is through mass vaccinations, as we have done with measles, smallpox and largely with polio.

A population has achieved herd immunity when a large enough percentage of individuals become immune to a disease. When this happens, infected people are no longer able to transmit the disease, and the epidemic will burn out.

As a professor of behavioral and community health sciences, I am acutely aware that mental, social and economic health are important for a person to thrive, and that public health measures such as social distancing have imposed severe restrictions on daily life. But based on all the research and science available, the leadership at the University of Pittsburgh Graduate School of Public Health and I believe this infection-based approach would almost certainly fail.

Dropping social distancing and mask wearing, reopening restaurants and allowing large gatherings will result in overwhelmed hospital systems and skyrocketing mortality. Furthermore, according to recent research, this reckless approach is unlikely to even produce the herd immunity that’s the whole point of such a plan.

Vaccination, in comparison, offers a much safer and likely more effective approach.

A graphic showing a collage of blue paper faces with a few isolated red faces
When enough of a population is immune to a virus, the immune people protect the vulnerable.
Wildpixel/iStock via Getty Images

An uncertain path to herd immunity

Herd immunity is an effective way to limit a deadly epidemic, but it requires a huge number of people to be immune.

The proportion of the population required for herd immunity depends on how infectious a virus is. This is measured by the basic reproduction number, R0, how many people a single contagious person would infect in a susceptible population. For SARS-CoV-2, R0 is between 2 and 3.2. At that level of infectiousness, between 50% and 67% of the population would need to develop immunity through exposure or vaccination to contain the pandemic.

The Great Barrington Declaration suggests the U.S. should aim for this immune threshold through infection rather than vaccination.

To get to 60% immunity in the U.S., about 198 million individuals would need to be infected, survive and develop resistance to the coronavirus. The demand on hospital care from infections would be overwhelming. And according to the WHO estimated infection fatality rate of 0.5%, that would mean nearly a million deaths if the country were to open up fully.

The Great Barrington Declaration hinges on the idea that you can effectively keep healthy, infected people away from those who are at higher risk. According to this plan, if only healthy people are exposed to the virus, then the U.S. could get to herd immunity and avoid mass deaths. This may sound reasonable, but in the real world with this particular virus, such a plan is simply not possible and ignores the risks to vulnerable people, young and old.

You can’t fully isolate high-risk populations

The Great Barrington Declaration calls for “allowing those who are at minimal risk of death to live their lives normally … while protecting those who are at highest risk.” Yet healthy people can get sick, and asymptomatic transmission, inadequate testing and difficulty isolating vulnerable people pose severe challenges to a neat separation based on risk.

First, the plan wrongly assumes that all healthy people can survive a coronavirus infection. Though at-risk groups do worse, young healthy people are also dying and facing long-term issues from the illness.

An older woman in a mask reaching to grab a can of food at a grocery store.
Grocery stores have been giving older and at-risk shoppers time to shop away from other people, but knowing whether the store employees are infected is not easy.
AP Photo/Sue Ogrocki

Second, not all high-risk people can self-isolate. In some areas, as much as 22% of the population have two or more chronic conditions that put them at higher risk for severe COVID-19. They might live with someone in the low-risk group and they still must shop, work and do the other activities necessary for life. High-risk individuals will come in contact with the low-risk group.

So can you simply guarantee that the low-risk people who interact with the high-risk group are uninfected? People who are infected but not showing symptoms may account for more than 30% of transmission. This asymptomatic spread is hard to detect.

Asymptomatic spread is compounded by shortcomings in the quality of testing. Currently available tests are fairly good, but do not reliably detect the coronavirus during the early phase of infection when viral concentrations can be low.

Accordingly, identifying infection in the low-risk population would be difficult. These people could go on to infect high-risk populations because it is impossible to prevent contact between them.

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Sweden’s herd immunity failure

Without sharp isolation of these two populations, uncontrolled transmission in younger, healthier people risks significant illness and death across vulnerable populations. Both computer models and one real-world experiment back up these fears.

A recent U.K. modeling effort assessed a range of relaxed suppression strategies and showed that none achieved herd immunity while also keeping cases below hospital capacity. This study estimated a fourfold increase in mortality among older people if only older people practice social distancing and the remainder of the population does not.

But epidemiologists don’t have to rely on computer models alone. Sweden tried this approach to infection-based herd immunity. It did not go well. Sweden’s mortality rate is on par with Italy’s and substantially higher than its neighbors. Despite this risky approach, Sweden’s economy still suffered, and on top of that, nowhere near enough Swedes have been infected to get to herd immunity. As of August 2020, only about 7.1% of the country had contracted the virus, with the highest rate of 11.4% in Stockholm. This is far short of the estimated 50%-67% required to achieve herd immunity to the coronavirus.

Two gloved hands holding a syringe and vaccine vial.
Vaccines offer a safe pathway to immunity for both the healthy and the vulnerable.
AP Photo/Hans Pennink, File

Exposure versus vaccination

There is one final reason to doubt the efficacy of infection-based herd immunity: Contracting and recovering from the coronavirus might not even give immunity for very long. One CDC report suggests that “people appear to become susceptible to reinfection around 90 days after onset of infection.” The potentially short duration of immunity in some recovered patients would certainly throw a wrench in such a plan. When combined with the fact that the highest estimates for antibody prevalence suggest that less than 10% of the U.S. population has been infected, it would be a long, dangerous and potentially impassable road to infection-based herd immunity.

But there is another way, one that has been done before: mass vaccination. Vaccine-induced herd immunity can end this pandemic the same way it has mostly ended measles, eradicated smallpox and nearly eradicated polio across the globe. Vaccines work.

Until mass SARS-CoV-2 vaccination, social distancing and use of face coverings, with comprehensive case finding, testing, tracing and isolation, are the safest approach. These tried-and-true public health measures will keep viral transmission low enough for people to work and attend school while managing smaller outbreaks as they arise. It isn’t a return to a totally normal life, but these approaches can balance social and economic needs with health. And then, once a vaccine is widely available, the country can move to herd immunity.The Conversation

Steven Albert, Professor and Chair of Behavioral and Community Health, University of Pittsburgh

This article is republished from The Conversation under a Creative Commons license. Read the original article.

How could wearing a mask help build immunity to COVID-19? It’s all about the viral dose


Larisa Labzin, The University of Queensland

People infected with SARS-CoV-2, the virus that causes COVID-19, can spread the virus when they speak, sing, cough, sneeze or even just breathe. Scientists think face masks help limit virus spread by protecting everyone else from the infected wearer. As a result, face maks are now mandatory in many cities, states and countries to limit the spread of COVID-19.

People typically wear surgical, cloth or other face coverings that don’t completely prevent the virus from infecting the wearer, though medical grade surgical masks do appear to offer more protection. Nonetheless, these don’t have the same level of protection as N95 or P2 “respirator” masks worn by many health-care workers. Additionally, how we wear the mask matters, as touching it often and not completely covering the nose and mouth renders it ineffective.

While these face coverings may not completely prevent us from getting infected with COVID-19, they probably reduce the number of virus particles we inhale — the “viral dose”. Scientists think a lower viral dose can reduce the severity of the disease we get. Indeed, where universal face masking is implemented, a much higher proportion of new infections with COVID-19 are asymptomatic.

Could this lower viral dose help us build some immunity to the disease? Two researchers from the University of California have raised this possibility, writing in the prestigious New England Journal of Medicine. Although the theory hasn’t been proven yet.

The dose makes the poison

How much virus we are initially infected with is a key determinant of how sick we get, according to evidence from other viruses and animal studies. We also know this is true in hamsters that have been experimentally infected with SARS-CoV-2.

Imagine if you touch a door handle that happens to have one virus particle on it, and then touch your nose and breathe that particle in. You will be infected with that one virus particle. One estimate, published in the Lancet, suggested one SARS-CoV-2 virus particle will have replicated to make nearly 30 new virus particles in 24 hours. Those 30 new particles can then go on to infect 30 more cells, giving rise to 900 new particles in the next 24 hours or so.

Now imagine someone sneezes right in your face and you inhale 1,000 virus particles. After one round of replication you could have 30,000 particles, and then 900,000 in the round after. In the same period of time your body could be dealing with 1,000 times more virus, compared to the first scenario.

How different types of masks work to block droplets from talking, coughing and sneezing (Thorax).

Once the immune system detects the virus, it has to race to get it under control and stop it replicating. It does this in three main ways:

  • telling our cells how to disrupt viral replication

  • making antibodies that recognise and neutralise the virus to stop it infecting more cells

  • making T cells that specifically kill virus-infected cells.

While the first step is relatively quick, creating specific antibodies and T cells takes days or even weeks. Meanwhile, the virus is replicating over and over again. So the initial dose of virus really determines how much of the body the virus has infected before the immune system kicks fully into gear.

What about for long-term immunity?

The more virus there is, the bigger the immune response has to be to control it. And it’s the immune response that actually causes the symptoms, like fever. In an asymptomatic infection, we think the immune system has probably managed to get the virus under control early on, so the immune response itself is possibly smaller, and so we won’t see any symptoms.

We also think many cases of very severe COVID-19 might really be a result of the immune system overreacting. This is why the steroid treatment dexamethasone, which suppresses the immune response, shows promise in treating severe cases (but not mild ones).




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After we clear an infection, we keep some immune cells around in case we get infected again. These are B cells, which produce antibodies specific to SARS-CoV-2, and T cells, which kill virus-infected cells. This is also the premise behind vaccination: we can trick the immune system into making those SARS-CoV-2 specific cells without having been infected.

Because face masks might allow a small number of virus particles through, wearers might be more likely to get asymptomatic infections. This might be enough to protect them from future infection with SARS-CoV-2. So if we are in a situation where there is high community transmission, and we can’t always maintain physical distance, wearing a face mask might be a factor that helps us in the long run.

It’s another argument in favour of masks

While this sounds promising, there’s still a lot we don’t understand. We don’t know yet whether an asymptomatic infection would generate enough immunity to guard against future infection — or if this is even measurable.

Viral dose is likely to be just one factor among many that determines how sick someone gets with COVID-19. Other factors include age, sex, and other underlying conditions. Finally, even with asymptomatic infections, we don’t know yet what the long term effects of COVID-19 are. It’s best to avoid getting COVID-19 altogether if possible.

Nevertheless, this is yet another reason to keep wearing face masks. As many cases of COVID-19 are asymptomatic, we could still be transmitting the virus even without symptoms. That’s why wearing a mask is a responsible thing to do, even if we feel fine.




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The Conversation


Larisa Labzin, Research Fellow, Institute for Molecular Bioscience, The University of Queensland

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Immunity to COVID-19 may not last. This threatens a vaccine and herd immunity


Nigel McMillan, Griffith University

How is the world going to go back to the days when we could grab a coffee, see a movie, or attend a concert or footy game with anyone?

Opinion suggests there are two options: an effective vaccine, or herd immunity via at least 60-80% of people becoming infected. Either one of these options requires that people become immune to SARS-CoV-2, the coronavirus that causes COVID-19.

An important new study released online this week could have a large bearing on how our future looks in 2021 and beyond.

It suggests our immunity to SARS-CoV-2 does not last very long at all — as little as two months for some people. If this is the case, it means a potential vaccine might require regular boosters, and herd immunity might not be viable at all.




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Immunity dwindles quickly

Antibodies are an important part of our immune system that mainly work by physically binding to virus particles and stopping them infecting cells. They can attach to infected cells to induce cell death in some cases.

We also have T cells, another part of the immune system that is much better at recognising and killing virus-infected cells. But for COVID-19, antibodies are important in the lungs because T cells aren’t good at getting to airways where the virus first invades.

A conceptual illustration of antibodies attacking the COVID-19 virus.
Antibodies attach on to viruses and prevent them from infecting our cells.
Shutterstock

The newly released research, from Katie Doores and her team at Kings College London, looked at how long the antibody response lasted in people who had COVID-19. It has been submitted to a journal but hasn’t been peer-reviewed, so it must be treated with some caution.

Of the 65 patients studied, 63 produced antibody responses. The important measurements in the study relate to how good the response is. This is measured in the lab by putting patients’ blood serum together with infectious SARS-CoV-2 virus and seeing whether the virus can infect cells in a lab dish. This is called a “neutralisation assay”, and here the results were good.

Around 60% of people produced a very potent neutralisation response that stopped virus growing in the lab cells.

Finally, the researchers measured how long the antibody response lasted. This is the most important data. Unfortunately, antibodies levels began falling after day 20 and only 17% of patients retained a potent level at day 57. Some patients completely lost their antibodies after two months.

This suggests our immune response to SARS-CoV-2 may be lost much faster than we might have hoped, and people might thereafter be susceptible to reinfection with the virus.




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One vaccine might not be enough

It therefore follows that COVID-19 vaccines may not be as effective as we hope. The fact antibody levels reduce over time is normal, but this typically happens much more slowly. Antibody responses against the mumps, measles and chickenpox viruses last for more than 50 years. A tetanus vaccination wanes more quickly but still lasts 5-10 years before a booster is needed.

So why is this happening? It comes down to the nature of the SARS-CoV-2 coronavirus itself. The four normal strains of coronaviruses that cause common colds in humans also fail to prompt a long-lasting immune response, with most people losing antibodies completely after 6-12 months. Coronaviruses in general seems to be particularly good at not being well recognised by our immune system. Indeed, a feature of common cold coronaviruses is that people get reinfected by them all the time.

SARS, another coronavirus which caused a pandemic in 2003, seems to produce a slightly longer antibody response, lasting up to three years. It’s still a long way short of a lifetime, but it perhaps helps explain why the virus disappeared in 2003.

Herd immunity might be in trouble

So herd immunity may not be the solution some think. This is because if immunity is short-lived, we will be in an ongoing cycle of endless reinfection. For herd immunity to be effective we need a high percentage (perhaps more than 60%) of people to be immune at any one time to disrupt chains of transmission. This can’t happen if a lot of reinfection is occurring.

The hope is vaccines will give much stronger and longer lasting immune responses to the virus than getting and recovering from COVID-19 itself. Indeed, the first vaccine candidates from Pfizer and Moderna, reported in early July, show very strong immune responses.

However, these studies only reported out to 14 and 57 days, respectively, after vaccinations were completed. They don’t tell us whether there is a long-lived response that we would need for a vaccine to be truly protective. Phase 3 trials designed to measure this are due to report in December 2020, so watch this space.

While we wait, we should reflect on the fact that although the results of the Kings College study are in one sense disappointing news, this knowledge adds to the truly remarkable scientific progress we have made in understanding a virus that only emerged in December 2019.


This article is supported by the Judith Neilson Institute for Journalism and Ideas.The Conversation

Nigel McMillan, Program Director, Infectious Diseases and Immunology, Menzies Health Institute, Griffith University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

The costs of the shutdown are overestimated — they’re outweighed by its $1 trillion benefi



Shutterstock

Richard Holden, UNSW and Bruce Preston, University of Melbourne

As Australia begins to relax its COVID-19 restrictions there is understandable debate about how quickly that should proceed, and whether lockdowns even made sense in Australia in the first place.

The sceptics arguing for more rapid relaxation of containment measures point to the economic costs of lockdowns and appeal to the cold calculus of cost-benefit analysis to conclude that the lives saved by lockdowns don’t justify the economic costs incurred to do so.

Their numbers don’t stack up.

To be able to weigh the value of a life against the economic costs of forgone output from lost jobs and business closures, requires placing a dollar value on one person’s life. This number is called the value of a statistical life.




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In Australia, the Government generally uses a value of A$4.9 million. The United States uses a value of US$10 million.

What are the benefits of the shutdown? This is the value of lives saved plus any indirect economic or health benefits. Lives saved are those excess lives that would be lost if government relied on a strategy that allowed enough people to get infected to result in so-called herd immunity.

How many extra lives would be lost under this second strategy?

To answer this, we need assumptions about the virus.

The lives lost if we let it rip

The initial reproduction rate of the virus, R0, was thought to be about 2.5. This means that every 2 people infected were likely to infect another 5; producing an average infection rate per person of 2.5.

Herd immunity for COVID-19 is estimated to require roughly 60% of the population be infected before the curve begins to flatten and the peak infections fall.




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This happens when the reproduction rate, R0, falls below one. Because of subsequent new infections, the total number infected over the course of the pandemic is closer to 90%.

Given a population of 25 million people and assuming a fatality rate of 1%, this would produce 225,000 deaths.

An assumption of a 1% fatality rate is low from the perspective of those making decisions at the onset of the pandemic, at a time when crucial and reliable data were missing.

Those lives are valued at $1.1 trillion

Converting those fatalities to dollars using the Australian value of a statistical life of A$4.9 million per life yields a cost of A$1.1 trillion.

In rough terms, that’s the amount we have gained by shutting down the economy, provided deaths do not skyrocket when lockdown measures are relaxed and borders re-open.

It is about three fifths of one year’s gross domestic product, which is about A$1.9 trillion.

What are the costs of the shutdown?

These are the direct economic costs from reduced economic activity plus the indirect social, medical, and economic costs, all measured in terms of national income.

A starting point is to take the lost income that occurs from the recession that has probably already begun.

What will the shutdown cost?

Let’s assume that the downturn results in a 10% drop in gross domestic product over 2020 and 2021 – about $180 billion – consistent with IMF forecasts of a fall in GDP of 6.7% in 2020 and a sharp rebound of 6.1% growth in 2021, and comparable to the Reserve Bank of Australia’s forecasts in the latest Statement on Monetary Policy.

Comparing this cost from shutting down – about $180 billion – to the benefit of $1,103 billion – makes the case for shutdown clear.

But this calculation grossly overestimates the costs of the shutdown.

The recession is a consequence of both the shutdown and the pandemic.

We need to attribute costs to each.

Most of the economic costs of the recession are likely to be due to the pandemic itself rather the shutdown.

Many costs would have been borne anyway

Even before the shutdown, economic activity was in decline.

Both in Australia and internationally air travel, restaurant bookings and a range of other activities had fallen sharply.

They were the result of a “private shutdown” that commenced before the mandated government shutdown.

Even in a country such as Sweden, where a shutdown has not been mandatory, there has been a more than 75% reduction in movement in central Stockholm and a more than 90% reduction in travel to some domestic holiday destinations.




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To be generous, let’s assume the costs attributable to the government-mandated part of the shutdown are half of the total costs, making their cost A$90 billion.

In reality, they are likely to be less, one important study suggests much less.

It is hard to imagine a much bigger private shutdown not taking place had the government decided to simply let the disease rip until its spread was slowed by herd immunity.

Support is not a cost

It is also important to note that the government’s spending of A$214 billion to support the economy during the shutdown is a transfer of resources from one part of society to another rather than a cost.

It creates neither direct costs nor benefits for society as a whole, other than the economic distortions coming from raising the revenue to service the spending.

With long-term government bond rates near 1% (less than inflation), the total cost of distortions is likely to be tiny.

Of course, this discussion simplifies what are incredibly complex social, health and economic questions. There are clearly further costs, from both relaxing restrictions and keeping them in place.

Other costs are not that big

These costs are worthy of serious study and should rightly be part of a comprehensive public policy discussion. But looked at through the lens of a cost-benefit analysis these combined effects are likely to be small relative to the value of preventing mass death.

Among them are the incidence of mental health problems and domestic violence under lockdowns. They are important concerns that should be addressed by targeted and well-designed programs.

Weighing against that is evidence that economic crises are associated with declines in overall mortality rates.




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While suicides rise, total mortality, including deaths from heart attacks and workplace and traffic accidents, falls.

In the specific case of this pandemic there is survey evidence based on respondents from 58 countries suggesting that strong government responses to the pandemic have been reducing worry and depression.

Also, we have to acknowledge that recessions and educational disruption have health and economic costs that are unequally spread.

The shutdown disproportionately impacts more-disadvantaged people including short-term casual workers, migrant workers, those with disabilities and the homeless.

The most-disadvantaged suffer, either way

This skewing will also be present in the herd immunity option. As New York City makes clear, a rapid spread of the disease also disproportionately impacts disadvantaged communities. One can only speculate about the disease burden should some of our remote indigenous communities get exposed.

To this we should add further achievements of the shutdown:

  • elimination of mental trauma and grief from losing our loved ones

  • avoiding the costs of possible longer-term implications of the disease, which we still know little about

  • avoiding a collapse in the capacity of the health system to deal with other emergencies through the sheer numbers of COVID-19 infected combined with staff shortages due to illness

Those advocating cost-benefit analysis of this kind have to apply the principle systematically. It is difficult to see how the total of these sorts of considerations on each side of the ledger could compare to the benefit of lives saved. They will be an order of magnitude, if not two, smaller.

$90 billion, versus $1.1 trillion

In the cold calculus of cost-benefit analysis, a highly pessimistic view of the economic costs of Australia’s shutdown comes to around $90 billion.

It is a small price to pay compared to the statistical value of lives the shutdown should save, around A$1.1 trillion.

It produces a simple message. The shutdown wins.




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The question we now face is how quickly to relax restrictions. Here, too, there are costs and benefits, and we need to be mindful of the economic cost of a second-wave outbreak, plus mortality costs of disease spread before effective treatments or vaccine become available.

And in all of this bean counting, we should remember that putting a price tag on human life is sometimes unavoidable – such as when a doctor with access to only one ventilator has to choose between two patients.

But we shouldn’t mistake necessity for desirability. We should seek to avoid needing to make such wrenching choices whenever possible.


Dr Jen Schaefer of the Royal Children’s Hospital Melbourne assisted with the preparation of this piece.The Conversation

Richard Holden, Professor of Economics, UNSW and Bruce Preston, Professor of Economics, University of Melbourne

This article is republished from The Conversation under a Creative Commons license. Read the original article.

The ‘herd immunity’ route to fighting coronavirus is unethical and potentially dangerous



Simon McSweeney/Flickr

Arindam Basu, University of Canterbury

As most of the world tries to suppress the coronavirus spread, some countries are going it alone – trying to manage the pandemic through so-called “herd immunity”.

Herd immunity means letting a large number of people catch a disease, and hence develop immunity to it, to stop the virus spreading.

The Netherlands reportedly plans to use herd immunity to combat the coronavirus epidemic, just as Britain retreats from such plans after warnings it could lead to 250,000 deaths.




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A “herd immunity” strategy has been criticised by the World Health Organisation, which said far greater action is required. Other health experts say the approach is experimental at best, and dangerous at worst.

So can herd immunity protect us from the coronavirus, and are countries wise to adopt it?

British Prime Minister Boris Johnson was criticised for seemingly adopting a herd immunity strategy.
EPA

First, let’s understand immunity

Our bodies fight infectious diseases such as coronavirus through our immune systems. The body produces antibodies in response to intruder organisms to fight and remove them.

Once the body has fought off a disease, it retains a “memory” of the germ, and how to fight it better and faster next time.

Once a person has developed immunity to a virus, they probably won’t catch it again. The theory behind herd immunity is that once a lot of people develop immunity to a virus, it will eventually stop spreading to people who haven’t yet caught it.

Herd immunity is more effective if a vaccine is available.
AAP/David Crosling

Number-crunching on herd immunity

Herd immunity is essentially a numbers game.

It all rests on the basic reproduction rate – in other words, how many new infections each case will generate.

A rate with a value of 1 would mean that one person can pass it on to at least one other person. The higher this number, the more infections from that one case. So to end the spread, this number will need to drop below 1.

The reproduction rate for coronavirus is between 2 and 3.




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As infection spreads, the pool of susceptible people shrinks as more develop immunity. Herd immunity aims to lower the number of susceptible people to the point where the reproduction rate drops below 1 and the spread of infection stops.

In the case of measles, 95% of people need to be immune for infection to cease. For coronavirus, I calculate this figure is around 40%, based on a reproduction rate of 2.6. So, if about 60% people are immune to the infection, this is sufficient herd immunity to stop coronavirus spreading.

(There have been a few reports of people becoming infected with coronavirus twice, but they haven’t been substantiated in peer-reviewed research, so can be discounted for now.)

An image showing the main elements of coronavirus.
Wikimedia

So is herd immunity a good plan?

On the face of it, a herd immunity strategy might seem wise. But the absence of a coronavirus vaccine means it is very high-risk.

The best way to rapidly develop herd immunity is through vaccination. A vaccine delivers a small amount of a virus into the body, and the immune system learns how to fight it off without having to get sick. But we do not yet have a vaccine for coronavirus.

If vaccines are not available and the infection spreads, some people will develop a mild version of the disease and recover. But it is dangerous and unethical to rely on this method to combat the disease.




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First, the intermediate and longer term consequences of coronavirus are not yet known. And second, while some people are not badly affected by the disease, under a herd immunity strategy they could still pass the virus to elderly people who are at high risk of dying from it.

One expert analysis found that creating herd immunity in the UK would require more than 47 million people to be infected. With a 2.3% fatality rate and a 19% rate of severe disease, this could result in more than a million people dying and a further eight million needing critical care.

A coronavirus patient being transported to hospital in Italy.
EPA

What should we be doing?

Let’s say Australia and New Zealand relied on herd immunity. Now let’s assume, conservatively, that 10% of the population were infected – that’s 500,000 New Zealanders and 2.5 million Australians. Over a short period, those numbers would disastrously overwhelm the nations’ health systems.

The safest public health strategy is to prevent the onset of coronavirus at all costs. This would buy the health system time, “flattening the curve” so hospitals were not inundated with cases all at once.

This is why it’s so important to control movement across our borders, impose self-isolation, restrict public gatherings, trace the contacts of existing cases and isolate those with the virus. Australia and New Zealand are both now essentially following these measures. It might also be wise to screen passengers in departure terminals for signs of the virus, and test where necessary.

Also critical is educating the public on safe hygiene and ensuring supply of disinfectants, hand sanitisers, safe food, soap, and water, as well as access to services when needed. Now is also the time to take extra care of our elderly.

With these measures in place, we give ourselves the best chance of putting the coronavirus genie back in the bottle sooner rather than later, and minimising the number of deaths.The Conversation

Arindam Basu, Associate Professor, Epidemiology and Environmental Health, University of Canterbury

This article is republished from The Conversation under a Creative Commons license. Read the original article.

What is herd immunity and how many people need to be vaccinated to protect a community?



The vaccine coverage needed for herd immunity varies from disease to disease.
Ryoji Iwata/Unsplash

Hassan Vally, La Trobe University

The term herd immunity comes from the observation of how a herd of buffalo forms a circle, with the strong on the outside protecting the weaker and more vulnerable on the inside.

This is similar to how herd immunity works in preventing the spread of infectious diseases. Those who are strong enough to get vaccinated directly protect themselves from infection. They also indirectly shield vulnerable people who cannot be vaccinated.

There are various reasons a person may not be able to be successfully vaccinated. People undergoing cancer treatment, and whose immune systems are compromised, for instance, are impaired in their ability to develop protective immunity from all vaccines. Often, people who can’t be vaccinated are susceptible to the most serious consequences from being infected.

Another vulnerable group are babies. Infants under six months of age are susceptible to serious complications from influenza. Yet they can’t be given the flu vaccine as their immune systems are not strong enough.




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How does herd immunity work?

For a contagious disease to spread, an infectious agent needs to find susceptible (non-immune) people to infect. If it can’t, the chain of infection is interrupted and the amount of disease in the population reduces.

Another way of thinking about it is that the disease needs susceptible victims to survive in the population. Without these, it effectively starves and dies out.

If most of the population is immunised, the disease dies out.
NIAID, CC BY

What level of coverage provides herd immunity?

How many people need to be vaccinated to achieve herd immunity varies from disease to disease.

Measles can be transmitted through coughing and sneezing and the virus causing measles can survive outside the body for up to two hours. So it’s possible to catch measles just by being in the same room as someone who is ill if you touch a surface they’ve coughed or sneezed on.

In contrast, Ebola can only be spread by direct contact with infected secretions (blood, faeces or vomit) and therefore requires close contact with an ill person. This makes it much less spreadable.




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We can determine how contagious a disease is by tracking its spread throughout a population. In doing so, we can attribute each disease a reproductive number denoted by the symbol Ro. The bigger the Ro the more easily the disease is spread throughout the population.

If everyone who has a disease on average infects two people, the Ro for that disease is 2. This means the disease, relatively speaking, is not particularly contagious. However, if everyone who has a disease infects ten people on average, it would have an Ro of 10, which means it’s a much more contagious disease.

We can use the Ro for a disease to calculate the herd immunity threshold, which is the minimum percentage of people in the population that would need to be vaccinated to ensure a disease does not persist in the population. The more contagious a disease, the higher the threshold.

Measles is one of the most infectious diseases to affect humans with an Ro of 12-18. To achieve herd immunity to measles in a population we need 92-95% of the population to be vaccinated.

Current data indicates full vaccine coverage for five year olds in Australia is sitting at around the 95% level. However, vaccination rates in some communities have fallen below ideal levels, making them susceptible to measles outbreaks.

The overwhelming success of measles vaccinations means many people have no memory of what this disease looks like, and this has resulted in its effects being underestimated. Measles can cause blindness and acute encephalitis (inflammation of the brain), which can result in permanent brain damage.




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Herd immunity, or community immunity, as it’s sometimes called, is a powerful public health tool. By ensuring those who can be vaccinated do get vaccinated we can achieve herd immunity and prevent the illness and suffering that comes from the spread of infectious diseases.The Conversation

Hassan Vally, Associate Professor, La Trobe University

This article is republished from The Conversation under a Creative Commons license. Read the original article.