These days, studies heralding some hopeful — or horrifying — new finding about the coronavirus are multiplying nearly as fast as the bug itself. As medical researchers the world over give COVID-19 their undivided attention, each week brings a new smorgasbord of working papers that leave lay-observers either jubilantly awaiting the imminent reopening of America’s underground mud-wrestling rings or despondently preparing for another 18 months of awkward Zoom happy hours, depending on which items they happen to sample.
To help you get a better handle on the latest things we’ve learned about the novel coronavirus, and our prospects for vanquishing it, Intelligencer is assembling periodic rundowns of all the good and bad news that’s come our way. (You can check out last week’s list here.)
Critically, the findings described here are preliminary. Humanity has only had a few months’ experience with the virus formally known as SARS-CoV-2. Our understanding of it is partial and subject to change. So take the following with a grain of salt (but not, under any circumstances, an unprescribed dose of hydroxychloroquine).
The good news.
1) The coronavirus may not be able to get by without large public gatherings.
The novel coronavirus has been nearly as confounding to human reason as it’s been to the human immune system. Our species likes to fit threats into clear, cause-and-effect narratives in which human agency plays a decisive role. And we’ve managed to construct several credible morality tales about the COVID-19 pandemic (e.g., an ounce of preemptive lockdown is worth a pound of cure).
But the pandemic has routinely complicated these stories by casting chaos as a protagonist: Although decisions about when and how to implement lockdowns contributed to disparate outcomes between jurisdictions, a good amount of divergence has been ostensibly random. For example, despite resisting widespread closures of nonessential businesses for months after its first confirmed case of COVID-19, Japan has enjoyed one of the lowest per-capita coronavirus death rates of any affected country (which is especially remarkable given that Japan has the second-oldest population in the world). Meanwhile, policy alone can’t seem to explain why some of the world’s large, dense cities have seen mild outbreaks, even as others have been devastated. Which raises the question: Is there no guidance when random rules?
Happily, new research has yielded a theory that helps explain the pandemic’s most puzzling aspects — and just might allow us to curb the virus’s spread through means less onerous than total lockdowns.
All viruses thrive on large public events and individual “super-spreaders.” But the novel coronavirus appears to be unusually dependent on both. The media conversation about SARS-CoV-2 has popularized one key epidemiological variable — R, the average number of people an afflicted individual infects. Before social-distancing measures were enacted, the coronavirus had an R of about three. And yet, this average obscures the profound variation between individuals. Estimates vary, but multiple research teams believe that the typical COVID-19 patient does not infect a single other person, a reality that is concealed by the prolific transmission rates of so-called super-spreaders. In fact, according to a new study from the London School of Hygiene & Tropical Medicine (LSHTM), about 10 percent of coronavirus patients are responsible for 80 percent of all new infections. This means that the coronavirus’s high R is potentially mitigated by its low k — a variable that describes how reliant a disease is on clusters of infection in order to spread. Viruses with a high k, such as the 1918 influenza, can spread diffusely through a large number of individuals. Those with a low k — such as the novel coronavirus’s close relatives SARS and MERS — cannot sustain themselves without super-spreaders. This was one reason why both of those coronaviruses burned out quickly and never recurred. Research from the University of Bern suggests that the coronavirus has a slightly higher k than SARS or MERS but one that is much lower than that of the Spanish flu.
This finding makes some of the random disparities in outcomes easier to understand. A virus with a low k value needs a bit of luck to get off the ground. If such a bug gets itself into the right human — say, one who’s too committed to choir practice to let a cold keep them home — it can gain a foothold in a community. If it infects a bunch of lonely homebodies, meanwhile, it will die out before making its presence felt (as the novel coronavirus ostensibly did in France last December). If SARS-CoV-2 has a k as low as the LSHTM study claims, then it would need to be introduced to a new country four separate times before securing a 50/50 chance of infecting enough people to sustain a prolonged outbreak.
Of course, the virus’s odds of landing on a super-spreader aren’t determined by luck alone. The fewer mass (indoor) gatherings a society holds, the fewer opportunities SARS-CoV-2 will have to hit pay dirt. This could explain while partial reopenings haven’t produced giant surges in cases as of yet; Georgians still aren’t generally attending large concerts, conferences, or sporting events. It’s possible, then, that a combination of banning large gatherings — including those convened on a daily basis at open-plan offices and meatpacking plants — and encouraging ubiquitous mask-wearing will prove sufficient to contain COVID-19. Which is to say: We may be able to enjoy many forms of “nonessential” commerce without sparking a surge caseloads (though we may need to eat a bit less meat).
2) It is possible that a significant number of people who’ve never been infected with the novel coronavirus already possess some immunity to it.
In last week’s roundup, we featured a study that found that a survivor of SARS possessed an antibody that ostensibly confers immunity to COVID-19. This was auspicious for our odds of developing an effective novel-coronavirus vaccine since an antibody capable of neutralizing viruses as distinct as SARS and the COVID-19 bug should be versatile enough to neutralize all mutated versions of the latter.
This said, even if every SARS survivor were immune to the novel coronavirus, it would make little immediate difference epidemiologically, as only an infinitesimal fraction of humans were ever infected with SARS.
But SARS and MERS weren’t the only forerunners of our present affliction. Several common colds are also coronaviruses. And if a significant percentage of people who’ve recovered from such colds possess cross-reactive immunity to SARS-CoV-2, then the population liable to contract COVID-19 — and spread the novel coronavirus — would be smaller than previously feared.
A recent study from the Center for Infectious Disease and Vaccine Research and the La Jolla Institute for Immunology suggests that this might be the case. Examining blood samples taken between 2015 and 2018 (when the novel coronavirus was still just a twinkle in Satan’s eye), researchers found that roughly 50 percent of these blood-givers possessed “SARS-CoV-2-reactive CD4+ T cells” — which is to say, their immune systems appeared capable of immediately recognizing and combating the novel coronavirus. Since none of these individuals could have been exposed to SARS-CoV-2, the most likely explanation for their possession of such T cells is previous exposure to a common-cold coronavirus.
Now, this was just a single study of blood samples. It remains unclear how prevalent these T cells actually are in the general population and how effective they truly are in combating COVID-19. But it’s at least possible that SARS-CoV-2 will suffer a fate not entirely dissimilar to the 2009 H1N1 swine flu, whose spread was undermined by the “immunological head start” humanity had derived from similar influenza strains.
3) Coronavirus patients cease to be infectious two weeks after developing symptoms.
This was already conventional wisdom. But a new study from Singapore fortifies the consensus by finding that 100 percent of its 73 observed coronavirus sufferers ceased to have a viable virus in their bodies 11 days after the onset of symptoms.
4) Scientists appear to have identified biomarkers that can predict whether a COVID-19 patient will develop severe illness ten days in advance.
Most people who contract the novel coronavirus do not develop serious illness. Even among demographically vulnerable populations, there are wide disparities in individual outcomes. If it were possible to drill down beneath age and common comorbidities to even more fine-grained predictors of COVID-19 vulnerability, medical and public-health officials would be better able to shield those most at-risk.
A recent study in the journal Nature Machine Intelligence identifies such predictors. Researchers analyzed 485 coronavirus patients in Wuhan, China, using machine-learning tools to isolate biological characteristics unique to the subset of patients who ultimately perished from COVID-19.
They found that three biological markers are so predictive of mortality, they can signal whether a COVID-19 patient will develop life-threatening illness with 90 percent accuracy more than ten days ahead of time. The three so-called biomarkers, all of which can be measured using a single drop of blood, were:
1) Elevated levels of the enzyme lactic dehydrogenase (LDH).
2) Low levels of lymphocytes (i.e., white blood cells).
3) High-sensitivity C-reactive proteins, which are indicative of respiratory inflammation.
By widely testing for these biomarkers, medical professionals could separate patients who will experience COVID-19 as a bad cold from those who will experience it as a mortal threat long before the distinction becomes apparent to the patients themselves. This would allow hospitals to better concentrate resources and thus, theoretically, reduce COVID-19’s overall fatality rate.
5) The coronavirus’s mutations don’t appear to have made it more infectious.
Viruses evolve constantly. And SARS-CoV-2 is no exception: According to researchers at University College London (UCL), the novel coronavirus has produced 273 mutations; of these, 31 have become prevalent.
One nightmare scenario for SARS-CoV-2 is that it will evolve into something even more lethal and infectious, as the 1918 influenza virus did before its devastating second wave. Fortunately, a new study from UCL indicates that none of the 31 prevalent mutations of the novel coronavirus are more virulent than the original brand.
6) The evidence that people who contract the coronavirus develop immunity-conferring antibodies is steadily growing.
Last week’s roundup included multiple studies indicating that COVID-19 survivors develop neutralizing antibodies and thus face no immediate risk of reinfection (how long such immunity lasts remains unclear). Now, a study of 160 French doctors and nurses who contracted mild cases of COVID-19 finds that 159 possessed neutralizing antibodies 41 days after showing symptoms. This is significant because many have feared that mild cases of COVID-19 might be insufficient to confer immunity.
7) The story is in the sewer; keep your ear to the grate.
Most of the metrics we have for assessing COVID-19 outbreaks are lagging indicators. Since it takes several days for patients to develop severe symptoms — and often weeks to display life-threatening ones — confirmed cases and death counts tell us more about how widely the virus was circulating in the recent past than how prevalent it will be in the near future.
But researchers at Yale University believe they’ve discovered a metric that can predict major municipal outbreaks a week in advance — the concentration of the coronavirus in a city’s sewers.
The bad news.
1) Herd immunity will take a lot more time and death to achieve than Sweden had hoped.
Sweden decided to make itself into Europe’s control group by forgoing formal lockdown orders or the closure of nonessential businesses. Instead, the Swedes opted for a “herd immunity” strategy to battling the novel coronavirus: By keeping its most vulnerable people isolated — while allowing healthy young people to circulate freely (and contract COVID-19 prolifically) — the nation would accelerate the process of collective immunization against the virus, thereby suffering less economic damage in the short run and fewer COVID-19 deaths in the long run than all those overreacting sucker countries.
Things aren’t working out as planned. The Swedish economy has suffered roughly as severe a downturn as that of Denmark. And in recent days, it’s had the highest per-capita coronavirus death rate in Europe.
Until last week, defenders of the Swedish strategy could still argue that it might pay off eventually: The policy was never intended to minimize coronavirus deaths in the immediate term, after all. And if keeping things open gets Sweden to herd immunity faster than other countries do, then the strategy could yield an aberrantly high fatality rate in the early months of the pandemic but an exceptionally low one over its full duration.
Unfortunately for Sweden — and for anyone hoping America’s reopenings will get us to herd immunity in short order — a recent study of residents in Stockholm found that just 7.3 percent of people in the Swedish city possessed COVID-19 antibodies in late April.
As mentioned above, it is possible that cross-reactive immunity from the common cold could accelerate the achievement of effective herd immunity. But that remains a hypothetical. Meanwhile, multiple studies have now indicated that if herd immunity can only be won through 60 to 70 percent of a population contracting the novel coronavirus, then the path to such a resolution will be far longer and deadlier than many had hoped.
2) If Americans return to the office this summer, they could accelerate COVID’s spread; if they stay home, they could plunge whole cities into darkness.
Some hope that summer will provide America with the comprehensive COVID-19 containment plan the Trump administration hasn’t. But while there’s evidence that the virus isn’t a huge fan of heat and ultraviolet light, the warming weather may do less to inhibit COVID-19’s spread than the growing use of air conditioners does to facilitate it.
Researchers from the Guangzhou Center for Disease Control and Prevention discovered that 10 people from three different families had contracted COVID-19 after all had dined at the same restaurant. After conducting a thorough investigation and study of their cases, the team concluded that an AC unit in the eatery had concentrated its blast of air on an infected diner, blowing the unwitting super-spreader’s viral droplets across three adjacent tables, thereby sickening the other families. As New York’s Justin Davidson reports, this study is indicative of the broader epidemiological hazard posed by poorly ventilated AC systems in densely occupied public buildings.
For this reason, many firms will hesitate to fully reopen their offices this summer. And yet, if America’s white-collar workers stay at home en masse — and each run their personal air conditioners all day long — then there will be dark times ahead. As the Daily Beast reports:
[T]he power infrastructure in residential areas is typically designed to accommodate heavy use in the early mornings and evenings, with hours to cool off during the day. Consumption patterns in these districts have already changed during the crisis, with demand spiking in the daytime. Overall usage is already up by an average of 7 percent in New York City apartments, and by 15 to 20 percent in homes in California.
As the summer heat peaks, and juice-sucking air conditioners remain on through the afternoon, the risk of failure in aged transformers and other equipment increases.
“The fact that Lower Manhattan is using less power is not going to help to deliver power to people in Queens, many of whom for health reasons may be intolerant to high temperatures, and whose buildings are connected to a very old transmission line with limited margins to carry extra power,” said [assistant professor at New York University’s Tandon School of Engineering Yury] Dvorkin. “What’s going to happen this summer, if we have stay-at-home orders, if we have consumption which the grid was not designed to accommodate, it will push the system to its limits.”
3) Even as COVID-19 cases decline overall, rates of infection among the young may be holding steady.
Washington has “bent the curve” about as well as any U.S. state. But while its new case count has plummeted since early April, among Washingtonians ages 0 to 19, there has been “no decline in cases,” according to a new study from the University of Washington. In other words, declines have been concentrated among the old and vulnerable. This is a desirable demographic disparity in the immediate term. But since the young are less likely to become ill from the coronavirus — and thus less likely to ever get tested — the plateau in confirmed cases among young people may be the tip of a larger iceberg of youthful infection. Further, since the young tend to have close contacts with a wider pool of people than the elderly — and are more likely to carry the virus asymptomatically — the fact that cases are disproportionately concentrated among the young may heighten the probability that a new wave of infection emerges.
4) In the developing world, young people are dying from COVID-19 at unprecedented rates.
In wealthy countries, COVID-19 deaths have been overwhelmingly concentrated among the old. But as the novel coronavirus gains ground in less prosperous places, fatality rates are rising among the young. As the Washington Post reports:
In Brazil, 15 percent of deaths have been people under 50 — a rate more than 10 times greater than in Italy or Spain. In Mexico, the trend is even more stark: Nearly one-fourth of the dead have been between 25 and 49. In India, officials reported this month that nearly half of the dead were younger than 60. In Rio de Janeiro state, more than two-thirds of hospitalizations are for people younger than 49.
At present, this alarming trend appears more attributable to grotesque international inequalities than to any viral mutation: Due to high levels of extreme poverty and underfunded health systems, many young people who would recover from COVID-19 with proper medical care are dying in the developing world without it.
In its first months, the pandemic focused its fury on the parts of the world best prepared to contain it. If SARS-CoV-2 becomes more pervasive in poor countries, its fatality rate could surge. (And at present, the wealthy world is giving every indication that any coronavirus vaccine will go first to nations with the greatest means, not those with the greatest need.)
5) Trump’s favorite coronavirus treatment appears to make coronavirus patients more likely to die from their illness.
The U.S. president has so much faith in hydroxychloroquine as a panacea for coronavirus, he not only recommended its use over the objections of government scientists but also started taking it himself as a prophylactic against COVID-19 (even though there is no scientific basis for believing that the anti-malarial drug prevents infection from the coronavirus).
Unfortunately, a new study of 96,000 coronavirus patients across six continents found that COVID-19 sufferers who were treated with hydroxychloroquine died at higher rates than those who were spared Dr. Trump’s miracle tonic.
6) Even as America reopens, half of its states have uncontrolled coronavirus spread.
A study from the Imperial College of London suggests that 24 U.S. states have an R higher than one — meaning that, on average, every person infected with the novel coronavirus gives the bug to at least one other person.
Meanwhile, a separate, peer-reviewed study published in Health Affairs indicates that areas of the U.S. that refused to impose social-distancing orders saw 35 times greater spread of the novel coronavirus than those that did implement such orders.
Neither of these findings bodes well for America’s nascent reopening.
7) On a global level, the daily count of new coronavirus infections is as high as it’s ever been.
Worldwide, the number of new, confirmed coronavirus cases is growing by about 100,000 a day, which is the highest sustained rate of new infections we’ve seen since the pandemic began.
