Kamala Harris has a complicated record, but her zeal to support abortion and attack its opponents has been consistent
In the COVID-19 debates, one topic manages simultaneously to be the most and least controversial: “herd immunity.” The concept of herd immunity is uncontroversial, and simply states that when enough members of a population develop immunity to a virus, the bug will fizzle out for lack of people to infect. The controversy, though, echoes every child’s favorite road-trip question: Are we almost there yet?
Two developments have raised the question with new vigor. One is in Washington, where Dr. Scott Atlas has become the newest White House adviser on the coronavirus task force. Atlas advocated for herd immunity in his May Senate testimony, saying, “If infection is still prevalent, socializing among these low-risk groups [younger, healthy adults] presents the opportunity for developing widespread immunity and eradicating the threat.” (His recommendations assume viral spread among low-risk groups will remain largely confined to those groups and won’t have serious long-term health consequences.)
The second development was summarized by a recent Washington Post article: Researchers are now questioning where the threshold for coronavirus herd immunity actually lies. So at what point can we argue that we’ve reached herd immunity?
Viruses spread at different rates in different populations. In a March letter to the editor in the Journal of Infection, a Hong Kong–based team attempted to calculate the coronavirus herd immunity threshold for various countries. The authors started with the basic idea that the more easily the virus spreads within a given population, the further that population must be from the immunity threshold. They based this on estimates of Rt, a figure measuring the “effective reproductive number.” (Think of weeds in gardens: They spread freely in general, but they may spread even better—or worse—depending on their circumstances. An Rt value below 1.0 would mean weeds are decreasing.)
The Hong Kong team estimated the U.S. herd immunity threshold was 69.6 percent, assuming no masks or social distancing—meaning about 7 out of 10 Americans would need to get the coronavirus (and survive) in order to stop its spread.
However, a Brazilian team’s new study (not yet peer reviewed) argues that individual variation in susceptibility or exposure could lower the threshold for herd immunity. That’s an interesting hypothesis, and the logic behind it makes sense up to a point. Clearly people who spend much of their time in crowded indoor places, such as the unfortunate folks who “get every cold that goes around,” are at higher risk than others. But—there’s always a “but,” isn’t there?—the Rt already takes that into account: It’s a population-level figure, and it considers those susceptible people along with the happy souls whose immune systems (or introverted lifestyles) mean they seemingly haven’t caught a virus in years.
The Brazilian team argues that under optimal circumstances, herd immunity could require as little as 20 percent of the population to be immune. Wonderful news if true—but is it? And how close can we get to those optimal circumstances? The fact is, we can do things to change effective reproductive number: America’s calculated Rt value, for example, went from an extreme high of 3.8 in some states down to slightly above 1.0 with social distancing, masking, contact tracing, and full-then-partial shutdowns.
We thus end up in another good news, bad news situation. The good news is that being able to change Rt means we can also temporarily, by all working together, get the benefits of herd immunity—reduced case numbers, reduced deaths, sustained reopening—even without having enough people contract SARS-CoV-2 to obtain true herd immunity. This is how distancing, hand-washing, mask-wearing, contact tracing, and staying home have held Taiwan’s population of 23 million people to a total of seven COVID-19 deaths. The Taiwanese are not unusually immune to the coronavirus. They simply worked together to pull Rt down to a level where the virus couldn’t spread.
The bad news comes if we mistake the good news for a get-out-of-jail-free card. The virus hasn’t changed, and the outbreaks at college campuses show just how easily it still spreads. A vaccine should be mass-produced soon—God willing, within the next six months. Observing that Rt is currently low, or that the infection and death figures are more reassuring now, should encourage us to stay the course with measures like masking and social distancing, not abandon them prematurely.
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Several readers have written to inform us about Richard Bartlett, a Texas doctor and onetime congressional candidate who says he has discovered a “silver bullet” for COVID-19. His proposed cure? Inhaled steroids.
This would be world-changing news, probably deserving a Nobel Prize, if true. It would save thousands of lives, end the economic and social upheaval caused by preventive measures, and save billions of dollars on hospital treatments.
As the ancient Spartans famously said: “If.”
I can’t say with certainty Dr. Bartlett hasn’t discovered a cure, for the same reason he shouldn’t imply that he has: What he currently has is a hypothesis, one whose evidence is as yet too limited to conclude that the treatment works at all, much less that it works in most or all COVID-19 patients. We simply don’t know. So how could we find out whether it’s a blockbuster—or a bust?
Back in March, we discussed a statistic called the “number needed to treat” (NNT). The NNT is the number of patients we’d need to treat in order to expect a medicine to have the desired effect in one patient. For a perfect treatment that benefits every patient who receives it, the NNT is 1. For many common prescriptions, though—statins for prevention of a heart attack, for instance—the NNT is more in the range of 20 to 100. You’d need to treat 20 to 100 patients in order to benefit just one.
Many medical conditions and illnesses go away by themselves. Given the relatively high NNT of many treatments, it’s often hard for researchers to tease out whether a new treatment is improving patient outcomes, or whether those patients would have fared equally well without the treatment.
This timeless source of job security for research statisticians brings us back to Dr. Bartlett and his series of patients. According to CBS7, Bartlett says he’s treated “dozens” of COVID-19 patients and all have survived. Since most patients with COVID-19 do survive, it raises the question: Did his patients benefit from the steroids, or were they patients who would have survived anyway?
Answers are on the way: Oxford and the Queensland University of Technology are already investigating this idea with their STOIC (Steroids in COVID-19) clinical trial. Queensland University of Technology elaborates on its origins: Two researchers “had noticed early on in the pandemic that people with asthma and the chronic lung disease COPD were under-represented in the numbers of seriously ill COVID-19 patients.” This struck them as unusual, since you’d normally expect patients with sick lungs not to have an advantage against respiratory viruses. That made them wonder whether those patients’ inhaled steroid treatments might be what was helping them.
In light of the recent discovery that another corticosteroid can help in severe cases of COVID-19—but not in less severe disease—I’m very curious to learn what the STOIC trial will reveal. STOIC aims to reach a conclusion by September.
In the meantime, let’s not—pardon the pun—jump the gun in our search for a silver bullet.
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In the race to defeat the coronavirus, the finish line is the mass production of a safe, effective vaccine.
Just as Jonas Salk’s vaccine helped transform polio from feared menace to historical curiosity in most countries, a good vaccine against today’s coronavirus would restore the world’s confidence, both socially (potlucks! concerts! sports!) and economically. So where does the vaccine race stand now?
The U.S. federal government’s unprecedented Operation Warp Speed project involves building factories to produce yet-unproven vaccines. That will allow the vaccines to come to market quickly if studies bear out their effectiveness. The Food and Drug Administration is speeding up the normal multiyear approval process with a “rolling review” that evaluates safety data as it comes in. (Here’s an excellent graphical summary.) The FDA has decided that, to be approved, a vaccine must make people 50 percent less likely to contract coronavirus or must reduce symptoms by 50 percent.
The nearly 150 coronavirus vaccine research projects—as of the World Health Organization’s latest count—have the same goal, but differ in their methods: Should a vaccine use an inactivated strain of the now-circulating SARS-CoV-2? Or should it use another, less dangerous virus, genetically modified to appear similar enough to the coronavirus that it will fool the person’s immune system? What if the vaccine doesn’t use a virus at all, but rather a protein the virus makes, or the messenger RNA (“mRNA”) that encodes a protein?
The World Health Organization (WHO) lists 19 vaccine candidates as having started human clinical trials as of July 6—with 130 more in pre-clinical animal studies. (Clinical research typically begins in phase 1, involving dozens of participants, and progresses to phase 3, involving thousands.)
- WHO lists only one vaccine candidate as having started phase 3 trials: ChAdOx1-S vaccine, a modified adenovirus vector from the University of Oxford and AstraZeneca. Sinovac’s inactivated virus vaccine is also about to start recruiting patients in Brazil for its own phase 3 trial. (The New York Times says a Wuhan-based team has also started a phase 3 trial in the United Arab Emirates.)
- Moderna’s mRNA vaccine has reached phase 2, with phase 3 anticipated for later this month.
- Oddly, the only vaccine already approved for human use is still in phase 2: China has approved CanSino’s vaccine for use in its military. That’s a risky call: A May article in Nature Biotechnology pointed out that CanSino based its vaccine on an adenovirus called Ad5—a vector to which the author estimated 45 percent of Chinese are already immune. That means the vaccine likely wouldn’t work in almost half of the population.
- Six more candidates are in “phase 1/2” status, combining the first two stages of research by automatically proceeding with the highest vaccine dose that did not cause harmful side effects.
Thinking even further outside the box, an Australian-led team is investigating a long-known phenomenon in which the bacillus Calmette-Guérin (BCG) vaccine, used to prevent tuberculosis in the developing world, seems to boost immunity more generally. Could it reduce the chances of severe COVID-19 infection? This team had a head start, since BCG has undergone extensive study over the years. Since the only question is whether it protects against the coronavirus, the team went straight to a phase 3 trial.
If we count the repurposed BCG vaccine along with Oxford’s, Sinovac’s, and Moderna’s coronavirus-specific vaccines, the end of July will likely see four phase 3 trials progressing simultaneously—with several more planned in months to come. Even the first trials won’t finish until fall, and successful mass production doesn’t mean instantaneous availability. But accelerated approval and pre-built factories should limit delays if one or more of the candidates prove worthy.
“This is not the end. It is not even the beginning of the end,” as Churchill once said. “But it is, perhaps, the end of the beginning.”