The U.K. backed off on herd immunity. To beat COVID-19, we’ll ultimately need it.
Widespread immunity is essential for a successful vaccine, but establishing it could be difficult for the new coronavirus.
While countries around the world began to lock down workplaces, schools, and public gatherings in response to the rapidly spreading coronavirus, the United Kingdom’s initial strategy sent many into an uproar.
At first, the U.K. chose not to shut down large gatherings or introduce stringent social distancing measures. In a plan that surprised many in the medical community, officials instead described a plan to suppress the virus through gradual restrictions, rather than trying to stamp it out entirely.
The strategy, an attempt to build “herd immunity,” involved allowing “enough of us who are going to get mild illness to become immune,” Sir Patrick Vallance, the U.K. government’s chief scientific adviser, told Sky News on March 13.
If the risks of COVID-19 were not so high, it would technically be possible to bring about herd immunity by allowing the disease to run rampant through a population. However, evidence shows that scenario would lead to high rates of hospitalisation and need for critical care, straining health service capacity past the breaking point.
After new simulations of the outbreak from Imperial College London showed how badly hospitals would be overwhelmed, the U.K. suddenly reversed course on Monday and introduced new social distancing measures. By Friday, the Prime Minister had ordered all pubs, restaurants, gyms, and cinemas to close.
Still, the question of herd immunity’s role in slowing the coronavirus lingers because of how it might determine the success of vaccine development—and the chances that the virus may flare back up once social distancing policies end.
Getting ahead of the virus
Viruses are stealthy. They disguise themselves as they infect a host and penetrate that host’s cells, which gives them a head start over the body’s immune response. Once a cell recognises certain telltale signs of a pathogen, it throws out an alarm signal to the immune system. But because the virus has that head start, it still has time to replicate itself and infect a new host before the immune system can catch up.
Immune responses within a cell can take around 24 hours to trigger, says Elly Gaunt, a virologist at the University of Edinburgh’s Roslin Institute. A full-blown immune response can take another three days—which means that a respiratory virus like the flu, which can replicate in as little as eight hours, is way ahead of the game.
That’s why someone’s first experience with an infectious disease can be so nasty. The immune system is not so easily tricked a second time: When it’s beaten an invader once, it keeps a specialised weapons cache dedicated to that particular pathogen, ready to mount a high-speed reaction if it’s ever detected again. So, the second time the disease shows up in your body, the virus won’t have that handy head start.
People with immunity are “duds for transmission,” says Katie Gostic, a University of Chicago researcher who studies immunity to influenza. And when viral transmission can’t sustain itself an epidemic will slow down and end, she explains.
Herd immunity can only be reached when a precise proportion of a community becomes resistant to an infectious disease, says Yonatan Grad, an epidemiologist at the Harvard T.H. Chan School of Public Health. You can’t have just some herd immunity, he explains, in the same way you can’t be just a little bit pregnant.
To have herd immunity, each infected person must, on average, infect less than one person (though clearly, it’s not possible to infect half a person; if some infected people pass on the infection and others don’t, the average transmission rate will be less than one.) Once the transmission rate drops below one, a community has herd immunity. That won’t stop each and every case, but it will prevent the disease from spreading indefinitely.
Many of our lessons on herd immunity come from the measles, because it's so contagious. The more infectious a disease is, the more people who need to be immune to reach herd immunity. One person with measles, for instance, could infect up to 18 other people in a susceptible population. To get that transmission rate all the way down to less than one, almost everyone in the population needs to act as a buffer between an infected person and a new potential host. That’s why measles needs such a high rate of herd immunity—around 95 percent.
Research so far suggests that the coronavirus has a lower infection rate than measles, with each infected person passing it on to two or three new people, on average. This means that herd immunity should be achieved when around 60 percent of the population becomes immune to COVID-19.
The do’s and don’ts of making a herd
Vaccines create a weapons cache for a disease without the body ever having to fight off the disease itself, which is why herd immunity is something that’s generally pursued through vaccination rather than infection. For example, about 30 percent of measles cases have complications such as seizures, pneumonia, and encephalitis, resulting in about two deaths for every thousand cases in the U.S. Exposing a whole population to measles would be a dangerous way to cultivate herd immunity among the survivors.
But it’s not unheard of for herd immunity to emerge through disease transmission. The infamous “chicken pox party” is a way some parents have intentionally exposed their children to a disease that’s commonly less harmful in childhood than in adulthood.
“The problem with coronavirus is that no-one has had it before, regardless of age,” says Gostic of the University of Chicago. It’s almost as if chicken pox had just emerged for the first time, leaving adults more susceptible to the more severe cases that come with age, she explains.
Herd immunity also isn’t something that can work for any disease. It doesn’t matter how many people are vaccinated against tetanus, for example: If someone who isn’t vaccinated steps on a rusty nail, they can still get infected, because tetanus lives in reservoirs outside of the human body. An infection must be transmitted between people for herd immunity to have a protective effect.
Immunity also doesn’t always last that long. HIV mutates so quickly that it can actually evolve within a single person, says Jessie Abbate, an infectious disease expert at the Research Institute for Development in France. Swiftly mutating flu is also a moving target for immunity and vaccines, which is why each flu season’s vaccine needs to anticipate the strain that will circulate widely, she explains.
What does this mean for coronavirus?
Four other coronaviruses already circulate among humans, says Gaunt, and they all cause the common cold, since we don’t stay immune to those viruses for very long. If the novel coronavirus is similar, that means that people would need to be repeatedly vaccinated or infected for herd immunity to be sustained.
Some reports describe reinfections of the novel coronavirus in people who tested positive again after they had already recovered. It’s not clear, though, that these are actually cases of reinfection—it’s more likely that they can be explained by people continuing to shed the virus for a long time, and that the level of virus shedding fluctuates over time.
Rapid reinfection is, for now, “an outside possibility,” Abbate agrees. If people were able to get sick again really quickly, we wouldn’t see the rapid decline in case numbers that is happening in certain parts of the world. And it would go against almost every other virus that we’ve known about, she says.
Even if a successful vaccine is developed, there will always be a small proportion of people who are vaccinated but don’t develop immunity. And if immunity to this new coronavirus is short-lived and needs repeated vaccination, that would present some extra logistical challenges, Grad adds.
In the meantime, the best policy for controlling the spread of the coronavirus is social distancing, which is why many medical professionals were relieved when the U.K. government rapidly changed its strategy.
"We were expecting herd immunity to build,” Azra Ghani, an infectious disease researcher at Imperial College London, said in a press briefing on March 16. “We now realise it’s not possible to cope with that.”
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‘Hydroxychloroquine tea’ is being peddled as a coronavirus cure in Brazil. It's fake.
Though there’s no proof that hydroxychloroquine fights COVID-19, an Amazon tree is being tapped for its supposed remedy. That may be unsafe.
Red cinchona (Cinchona pubescens; also known as Cinchona cordifolia) produces quinine, the antimalarial compound behind chloroquine and hydroxychloroquine. Here is a hand-colored lithograph by Hanhart after a botanical illustration by David Blair from Robert Bentley and Henry Trimen's Medicinal Plants, London, 1880.
In the Facebook video posted on March 30, a man turns over a small plastic bag he’s holding, filled with tree bark shavings. He shows his followers that it’s labeled “quina tea” and explains how to prepare the drink he says will “immunise your body and fight COVID-19.”
The demand for the tea will be high, he says, and he urges everyone watching to buy theirs now. He’s not the only one who thinks this way—and that may be a big problem.
As scientists the world over search for a way to prevent and treat COVID-19, some Brazilians have turned to nature for a remedy. They’ve stumbled upon a family of plants known locally as quina, used often in the Amazon and other rural communities to combat malaria and other inflammatory conditions. The tree is thought to have inspired what would later become hydroxychloroquine, a medication being touted by both Brazilian President Jair Bolsonaro and U.S. President Donald Trump as a treatment for COVID-19, despite a lack of solid scientific proof. (Here's what you should know about experimental therapies for coronavirus.)
For decades hydroxychloroquine has been used against diseases such as malaria and lupus, despite side effects including cardiac toxicity. The two politicians’ promotion of the drug has launched a debate over whether the medication is safe for those trying to avoid poor outcomes with the coronavirus. On June 3, a study of 800 people in the New England Journal of Medicine reported no evidence that hydroxychloroquine is helpful in preventing COVID-19, the latest in a long line of research citing shortcomings with the drug.
What’s more, quina trees aren’t quite what these Brazilians think—and the tea being promoted in videos and messages across social media could do more harm than good.
Quina is born
The year was 1638. After visiting the Amazon rainforest in Peru, the Spanish countess of Cinchón fell ill with a high fever. She was treated by a local indigenous group with a bitter substance they called quina quina. To her delight, the fever receded and she was cured—of what we now know was malaria.
The remedy came from an Andean tree traditionally called quina, or china, that would later be given the genus name Cinchona in the countess’s honour. Europeans returned home with the plant and sold it as a medication known as “Jesuits’ powder.” More than four decades later, it would also save England’s King Charles II from malaria.
Quinine tree (Cinchona pubescens; also known as Cinchona succirubra). Hand-colored steel engraving by Debray after a botanical illustration by Edouard Maubert from Pierre Oscar Reveil, A. Dupuis, Fr. Gerard and Francois Herincq’s La Regne Vegetal: Flore Medicale, L. Guerin, Paris, 1864-1871.
It would be centuries before scientists discovered this particular variety of Cinchona was a source of quinine, which would later inspire synthetic drugs including chloroquine and hydroxychloroquine.
As Europeans continued to extract the Cinchona for the malaria-fighting molecule, the Peruvian tree was pushed to the brink of extinction. The following century, a call went out to find substitutes for the bark in the Brazilian Amazon. Several plants were found and also given the name quina.
They weren’t, however, sources of quinine.
Dangerous tree swap
No species in the Cinchona genus that produces quinine grows naturally in Brazil, says Maria das Graças Lins Brandão, a pharmacist and organic chemist specialising in medicinal plants at the Federal University of Minas Gerais’s Natural History Museum and Botanical Gardens.
Instead, these alternative trees contain other alkaloids—natural chemicals that are bitter like quinine, which likely convinced the Europeans that these plants would have the same medicinal properties.
To this day, however, many of the dozens of Brazilian quinas, often referred to as false quinas, haven’t been extensively studied.
“They’re full of chemical substances we know nothing about yet,” Brandão says. “A lot of them are toxic and shouldn’t be ingested at all.”
Cinchona succirubra, a variety of quina tree also known as Cinchona pubescens, on a government plantation in Sikkim, India, 1866. Cinchona trees are native to South America but were transferred to plantations in India, after Europeans colonists learned that its plant extracts could fight malaria.
Brandão and her team have created a database of Brazilian plants and are studying the DNA of barks being sold in open-air markets as quinas. Of the 36 samples they’ve taken so far, four are false quinas. The other 32 plants are completely unrelated to the Cinchona genus and their medicinal effects are unknown.
Even if the Brazilian quinas did contain quinine that could be extracted, that wouldn’t make their derivatives equal to hydroxychloroquine. While quinine is a naturally occurring compound, the active ingredient in hydroxychloroquine is synthetic and has a completely different chemical makeup.
“Plants don’t produce anything specifically for us,” says Vanderlan Bolzani, an organic chemist at São Paulo State University who specialises in the chemistry of natural products and medicinal plants. “They only produce what they need to defend themselves. And a lot of the time, what they produce is toxic.”
Moreover, while many people consider tea a safer choice than taking a medication produced by the pharmaceutical industry, that’s not always true. When adding a natural substance, like quina bark, to boiling water, it’s not only the desired substance that is extracted, but also all the other chemicals produced by the plant, which could lead to dangerous results. One piece of quina bark may not even be chemically the same as another piece, depending on where the two trees are grown.
“Depending on the season, a plant modifies itself. It stops producing some substances and starts producing others,” Bolzani says. “Who can guarantee that, in order to survive, to adapt, to regulate itself, that plant has produced the same chemical composition?”
Quinine itself has always been known to be toxic. Quinine pills are still used as an alternative treatment for malaria when the disease shows resistance to newer drugs, such as hydroxychloroquine. But its common side effects—blurred vision, hearing loss, nausea, vomiting, and confusion—can be severe. In 2006, the U.S. Food and Drug Administration stopped allowing the sale of over-the-counter quinine to treat night leg cramps, after reports of serious side effects and death.
Killing trees
As many people turn to fake quinine tea as an alternative treatment for COVID-19, there is also concern that the plants themselves could suffer.
“When you take the bark from a tree, it dies,” says Brandão. “So, by using these plants in this way, you’re not only possibly harming the health of the person drinking this tea, but you’re also harming the environment at the same time.”
Experts agree that plants like the Brazilian quinas could have other therapeutic properties—but whether they could treat a disease, including COVID-19, is unknown.
“The majority of the scientific discoveries of value that we have, going as far back as aspirin, come from inspirations from nature,” says Lauro Euclides Soares Barata, an organic chemist specialising in natural products at the Federal University of the West of Pará. “But we need more studies. A small study takes at least four years. We’ve only been dealing with this virus for four months. What we need is time.”