By Elise Wachspress with Tinyan Dada
If you haven’t been infected yet, congratulations, you’ve made it this far.
We’ve streamlined our grocery store visits, maintained a six-foot distance at all times, even bought or made patterned, reusable masks for the family. We have a COVID routine, but we’re still waiting for the magic switch that will make everything normal again.
Thousands of scientists and technicians around the world are working to develop vaccines—substances that train our immune cells to attack particular pathogens—to keep us from getting COVID-19. Scientists continue to find multiple strains of the SARS-CoV2 virus circulating in various populations; it is becoming clear we may need multiple vaccines. And how long will these protect us? Measles inoculation works pretty much forever, but that is a rarity.
Sadly, even the most effective vaccination programs won’t work for everyone: the very young, the old, and especially those with impaired immune systems, for whom they may even cause disease. Will these people have to live forever in a COVID-19 bubble?
Maybe not. If we can establish herd immunity—where enough of the population is resistant to the disease—all of us might be able to resume a normal life.
But how many is “enough”? In an article in Immunity last month, UChicago geneticist Luis B Barreiro, PhD and grad student Haley E Randolph lay out the many parameters affecting herd immunity. In the case of this novel coronavirus, potentially influenced by countless unknowns—social structure, population density and age, even the genetic vulnerabilities of particular ethnic groups—assessing the potential for herd immunity becomes particularly uncertain and complicated.
The starting point, says Barreiro and Randolph, is to identify the average number of new cases each infected person might cause. In a completely susceptible population, where no one has experienced the virus before, this average is designated as R0. But once people start becoming resistant—either by getting the disease or through a vaccine—the effective reproduction rate, Re, starts to go down. The goal of vaccination programs is to get Re down below one, meaning more people have the disease than are transmitting it, and the disease curve begins to arc toward zero.
In the case of COVID-19, R0 has so far been estimated across different populations to be anywhere from around two to nearly six. (All of these R0 estimates were generated of course, without anyone understanding whether or how many people without symptoms can transmit the disease.)
So, Barreiro and Randolph suggest, suppose we take an average of the average—this totally new pathogen is forcing everyone to make a lot of guesses—and settle on an R0 of three. Mathematically, that would mean that incidence of the infection would begin to decline when about 67 percent of the population was resistant, and we would have a start—no promises!—toward herd immunity.
Complicating these models further are super-spreader events, like when one person singing in a church choir inadvertently infected at least 52 people with the coronavirus. We know from experience with MERS or even measles that one person or a tiny group can sometimes drive an inordinate number of infections. We don’t yet know how common these events are with COVID-19, although we have now learned that forcefully expelled droplets are a major mode of transmission, so taking precautions like wearing a mask, singing only at home, or even speaking more softly can ostensibly reduce R0.
Another important unknown is how long antibodies to the coronavirus might last. A year? Two? Because this coronavirus is so new, we have little idea how long the resistance we build up—either from having the disease or getting a vaccine—might last. Either way, protecting the vulnerable will depend on maintaining herd immunity over time.
Barreiro and Randolph go on to explain how to assess the infection fatality rate—the proportion of infected people who die of the disease—a metric critical in assessing the cost to society. Without isolation strategies, they project that worldwide deaths could exceed 30 million. Of course, as was the case in Italy, timing is everything: the faster the infection rate builds, the less likely the health care system can care for all the infected, and the more people will die.
In summary, Barreiro and Randolph point out that herd immunity is likely to work in only concert with a viable vaccination strategy, spread broadly throughout the population. Sweden’s coronavirus strategy involved keeping restaurants and businesses open, hoping that if less vulnerable members of the population interacted out in the community, they would generate some degree of herd immunity. So far, only around six percent of Swedes have developed COVID-19 antibodies, leaving the rest of the population at risk for serious illness and death and Swedes persona non grata visitors to other European countries.
So, in the short term, we continue to embrace our COVID routine. It is not much fun, but it may save our lives and the lives of others.
Tinyan Dada is a second-year undergraduate student at UChicago.
