Here’s why COVID-19 isn’t seasonal so far
Human immunity and behavior may be more important than weather for driving seasonality
Senior Writer, Molecular Biology
The pandemic may no longer be a public health emergency, but plenty of my neighbors, friends and family are still having bouts and brushes with COVID-19.
Just this past summer, a relative got COVID-19 on a camping trip. One of my neighbors was sick. Another had no symptoms but kept his distance while a bright pink line appeared on his test strip each morning. He shouted updates across the street as we walked our dogs: “The line was a little fainter today.” “It’s gone.” And finally, “It’s been two days since the line disappeared.” We and the dogs rejoiced at the reunion.
In the fall and winter, the reports poured in again: coworkers stricken with the coronavirus; the sick neighbor’s family got COVID-19 in the fall long after he recovered; a friend got sick after visiting a relative and missed Christmas with her parents; another friend’s cousins tested positive just after spending the holidays together.
The experiences of the people in my circle mirror the peaks and valleys of contagion seen across the United States and other temperate zones of the world. All of this got me wondering if SARS-CoV-2, the coronavirus that causes COVID-19, will ever settle in to becoming a virus that primarily strikes during cold and flu season. Having a predictable season would make timing and formulation of vaccines easier. It might also convince people that it’s wise to take precautions like wearing a mask at certain times of year.
Some recent data suggest that, for now, COVID-19 may be a year-round problem, driven more by human behavior and immunity levels than weather patterns.
COVID-19 is an all-weather spreader
Many common respiratory viruses spread better in cold, dry weather (SN: 1/11/23). Like the flu viruses, SARS-CoV-2 is more stable when the temperature and humidity are low. But scientists didn’t know whether the stability of the virus in well-controlled lab conditions translated to better spread at certain times of year in the real world, says Vincent Munster, a virologist at the Rocky Mountain Laboratories in Hamilton, Mont., part of the U.S. National Institutes of Health.
Munster and colleagues set up experiments with hamsters as stand-ins for people. The researchers wanted to examine airborne transmission — the primary way COVID-19 spreads — without having to worry about other less likely possible modes of spread, such as large droplets or contaminated surfaces. So the team infected one hamster and put it in a cage 90 centimeters away from a cage housing an uninfected hamster. At that distance, only airborne viruses could reach the uninfected hamster.
The team tested a typical climate-controlled room temperature (22° Celsius, or about 72° Fahrenheit) with a comfortable 45 percent relative humidity. Other hamsters were tested in cooler 10° C temperatures mimicking fall and winter in many parts of the world. A third cohort of animals got the tropical treatment at 27° C and 65 percent relative humidity.
Those environmental conditions don’t affect airborne transmission of the coronavirus, the researchers report January 9 in npj Viruses. The virus spread between hamsters at similar rates across all the conditions tested.
“Most of the time, the environmental impact on these viruses is relatively limited because they only stay in the air for a relatively short time,” Munster says. He’s talking seconds to minutes rather than hours or days.
Aerosols can hang around in the air for hours, Munster and colleagues have previously shown, but infection probably happens much faster, he says. Usually, an infected person would breathe out an infectious virus and someone nearby would inhale it. There’s just not enough transit time for environmental conditions to have a big impact on viral spread in those cases.
For the researchers, Munster says, “the biggest question was, ‘Does that mean these viruses don’t have the propensity to becoming seasonal?’” He thinks the coronavirus may someday have a season, but the determining factor won’t be the calendar. Instead, people’s immunity to the virus — from vaccination, prior infections or both — and human behavior will determine when COVID season hits, he predicts.
It’s not strangers who create transmission danger
Another recent study addresses that human behavior component. Researchers at the University of Oxford analyzed data collected from a cell phone app that was used to notify people when they had been a contact of someone who tested positive for COVID-19. The team examined more than 7 million notifications issued during the study period from April 2021 to February 2022. The researchers wanted to know if they could accurately predict whether someone would catch COVID-19 from looking at how close people were to infected people and how long the sick and well were together.
People often think “stranger danger” poses the biggest risk of getting infected, but that’s not what the data say, says epidemiologist Christophe Fraser.
The app was set to notify people if they’d been less than two meters from an infected person for 15 minutes. “The risk of transmission was really quite low at that point,” he says. The probability of transmission rose 1.1 percent per hour of exposure and kept increasing with continued exposure over several days, Fraser and colleagues reported December 20 in Nature. Households made up only 6 percent of contacts but accounted for 40 percent of transmissions.
Brief, casual contacts with strangers, such as at the grocery store, accounted for a large number of contacts, but few infections. Instead, the person who poses the most danger is “somebody you’ve spent a lot of time with: You could have dinner with them, go to the cinema with them, or you live at home with them or you work next to them in an office,” he says. That’s because infected people are constantly breathing out the virus and you have a greater chance of getting infected the longer you’re exposed and the closer you are to the source.
Other respiratory viruses have seasons that are influenced by human behavior in addition to the weather, Fraser says. For instance, flu and respiratory syncytial virus (RSV) outbreaks tend to coincide with children returning to school after summer and winter breaks (SN: 8/12/21). Perhaps COVID-19 will also settle into a similar pattern, but it may take decades, he says.
Human behavior can also quash seasonal viruses, at least for a time: Social distancing, mask-wearing and other COVID-prevention strategies severely tamped down the number of flu and RSV infections in 2020 and 2021 (SN: 2/2/21). But the viruses rebounded once those restrictions were lifted.
Some of the rebound of those seasonal viruses researchers think is because of loss of collective immunity against the viruses, especially among young children who have no immunity and older people whose immune systems tend to be weaker. Immunity also wanes the farther you get from a booster shot or infection.
Changes in human immunity may be the major driver of COVID-19 seasonality in the future, says Fraser’s Oxford colleague Luca Ferretti. But that’s not what has happened so far.
Early in the pandemic no one was immune to the virus, so it could infect almost everyone. Once vaccines became available and many people had immunity from the shots or previous infections, the original strain of the virus could be stopped or slowed by the immune system.
If the coronavirus changed relatively slowly the way other respiratory viruses do, COVID-19 might have already become a seasonal illness. But the coronavirus continues to change fast, often in ways that help it barrel right past immune defenses and infect even those with prior immunity.
For instance, the JN.1 variant started appearing in the U.S. Centers for Disease Control and Prevention’s reports in October. As of January 20, it made up almost 86 percent of cases in the United States. The virus sent more than 30,000 people to the hospital in the week of January 7 to 13 alone.
So far, the biggest outbreaks of coronavirus happened when new variants, such as delta and omicron, that allow the virus to escape antibodies came along. No one knows whether the virus has such dazzling escape acts left in its bag of tricks.
Our immunity has shifted when we’re most infectious
In addition to protecting us from COVID-19, human immunity has changed when people may be most infectious. Early in the pandemic, people produced the most virus and were most infectious in the first few days after infection, sometimes even before symptoms started. Now, immunity from vaccines and previous cases of COVID-19 have pushed back the peak of viral production until about four days after symptoms start, researchers reported September 28 in Clinical Infectious Diseases.
The reason for the change comes from the immune system fighting the virus earlier in the infection and producing symptoms before viral replication really takes off, says Nira Pollock, a clinical diagnostics expert at Boston Children’s Hospital.
That’s a good thing. But it also may inadvertently lead to more infections because it can affect when people get a positive result on home tests. Getting a positive line on a home test requires producing enough virus for the test to detect. So with a delay in peak viral production, you might get a negative test result but actually have COVID-19 and be able to pass it to others. That’s why repeat testing is necessary if you have symptoms or have been exposed to someone who does.
“If you test negative on day one, you are not done,” Pollock says. “If you continue to be symptomatic, you should repeat your test, because it’s possible that your highest viral load will be on your fourth day of symptoms, or your third or your fifth.” Repeat testing “is the FDA recommendation. It’s on the box.”
Being able to mark COVID-19 season on the calendar would be nice. At least then we’d know if we need to don masks along with our hats and gloves or with our beachwear. And there wouldn’t be so much guesswork in timing vaccinations.
For now, though, the coronavirus is on its own ever-changing timetable. Whether it eventually settles into a seasonal virus may depend on us. The strength of our collective immune systems and our willingness to take precautions to not spread any illness to others may eventually wrestle it into seasonal submission.