When Will COVID-19 Become ‘Endemic’?
With pandemic fatigue becoming ever more intense, there is increasing speculation about when the SARS-CoV-2 virus, which causes COVID-19, might become “endemic” – a time when outbreaks will be more modest and manageable and we can “coexist” with the virus. That juncture has been described as when the virus has become “annoying but rarely deadly or disruptive.” Unfortunately, there are no quantitative milestones that tell us when we’ve arrived. It’s really a judgment by individuals and society, and prematurely concluding that we’ve reached endemicity and abandoning precautions can have perilous consequences.
Many observers cite influenza – the “flu” – as an example of an endemic infectious disease, so it’s useful to review its impacts. According to the Centers for Disease Control’s statistics, from 2012-2019 the flu virus annually caused about 31 million symptomatic illnesses, 400,000 hospitalizations, and 39,000 deaths in the U.S. Those high numbers are in spite of moderately good vaccines, with efficacy in the range of 40%-60%, and which need to be administered each year.
Apparently, that’s what we, as a society, consider manageable and acceptable; after all, we don’t impose lockdowns, mask requirements, or widespread vaccine mandates during the annual flu outbreaks.
It’s not quite that simple, however, because COVID-19 isn’t the same as the flu. For one thing, there’s the phenomenon of post-COVID-19 syndrome, or “Long COVID,” which is marked by signs or symptoms that persist for more than four weeks, and often much longer, after the diagnosis of infection. It’s still too soon to know what percentage of the millions of Americans infected with Omicron will progress to Long COVID, but if the incidence is anywhere near the 10%-30% following Alpha and Delta SARS-CoV-2 infections, our health care system will be overwhelmed (to say nothing of the suffering of afflicted individuals).
Leaving aside Long COVID, the price we are already paying for the possible progression of COVID-19 to endemic, from pandemic, is horrific. As of Jan. 22, about 134,000 COVID-19 patients were hospitalized nationwide, down 16% from two weeks earlier. As former CDC Director Tom Frieden posted on Twitter on Jan. 23, “On an individual basis, Omicron is comparable in severity to flu. But on a societal basis, Omicron is likely to be much worse, causing at least twice as many cases as a typical three-four month flu season in just a few WEEKS.”
Dr. Frieden’s observation has important, and ominous, implications. Although Omicron-infected patients have substantially lower rates of hospitalization, admission to intensive-care units, use of mechanical ventilation, and death, and hospital stays were shorter, its higher contagiousness and the vast numbers of infections have pushed up the absolute number of hospitalizations. Many hospitals, and particularly their emergency rooms and ICUs, have been pushed to the breaking point, and a new subvariant of Omicron called BA.2, appears to be more contagious than its predecessor. A recent study by Danish researchers found that 39% of people infected with the BA.2 subvariant were likely to infect others in their households, compared with 29% of those who were infected with BA.1. The data were gathered from 8,541 households in December and January in Denmark, where BA.2 has become the dominant strain.
In an article in Foreign Affairs, University of Minnesota epidemiologist Michael Osterholm and writer Mark Olshaker accurately described our plight:
[Healthcare systems] are suffering the loss of 10% to 30% or more of already overburdened and burned-out staffs. Breakthrough infections among vaccinated people are occurring at least five times as frequently as they did with Delta, and Omicron appears to infect children more than previous strains. The crush of patients has been so severe that in a number of U.S. states and countries around the world, health-care workers with mild cases of the disease have had to continue working through their illness.
Here’s what that translates to on the ground at one Los Angeles hospital: “Arriving at the emergency department of Martin Luther King Jr. Community Hospital, people are treated in field tents, hallways, cubicles, former administrative offices and ambulance bays. Many wait in the open air with coughs and sore throats to get tested for the coronavirus.” That sounds more like medical care in a poor developing country than in America’s second largest city.
But pandemics do end eventually. The Spanish Flu of 1918-1920 is thought to have killed 50 million to 100 million people worldwide, including an estimated 675,000 Americans – at a time when the U.S. population was only about a third as large as it is today. My father, who was a child at the time, remembers his school being closed and wagons stacked with corpses rumbling through the streets of Philadelphia. (The death toll in that city alone was 13,000.) Finally, the virus became unable to find many new targets, the pandemic subsided, and flu became the endemic, seasonal infection it is today.
We need to keep in mind that every SARS-CoV-2 infection results in viral replication, the creation of new mutants, and the opportunity for Darwinian evolution to test them for “fitness” – that is, for greater transmissibility and enhanced ability to evade immune defenses. As Dr. Céline Gounder, a professor and infectious disease expert at New York University’s medical school, said recently, “I would be very careful about jumping to the conclusion that after this Omicron surge, we’re going to hit ‘endemic,’ or we’ll all have enough immunity that it’s just a common cold. I just don’t think we know that right now.”
So, for now, the most prudent course is still to get vaccinated, boosted, and take other reasonable precautions to “flatten the curve” of infections. The fewer infections, the less viral replication, the fewer mutants, and the lower probability of a new, worse variant appearing. And the sooner we’ll be able to declare the end of the pandemic.
Henry I. Miller, a physician and molecular biologist, is a senior fellow at the Pacific Research Institute and the former founding director of the FDA’s Office of Biotechnology. He is the co-discoverer of a critical enzyme in the influenza virus.
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