Influenza vaccination campaigns here have taken on added urgency this year. As the Brazilian state heads into its colder months, people brace for the fall and winter flu season. And by vaccinating as many people as possible against influenza, medical professionals hope they’ll be able to more quickly identify coronavirus disease (COVID-19) in patients who have symptoms common to both viruses.

That distinction could be crucial. Of the Southern Hemisphere’s nations, Brazil has the most confirmed cases and deaths caused by the novel coronavirus, and São Paulo has the most cases in the country as of April 16. Now, as temperatures start to drop across the region, questions are swirling about the possibility that the coronavirus could be seasonal and winter could make the situation even worse.

Seasonality is hard to determine with germs, in part because there are no genetic signals for this trait. Also, this coronavirus strain, known officially as SARS-CoV-2, is so new that there’s not yet enough data to say anything conclusive.

“It probably is a seasonal virus, just like other respiratory viruses, but in this first moment of propulsion, it’s still difficult to know how it will behave,” says Ana Paula Sayuri Sato, an epidemiologist at the University of São Paulo’s School of Public Health.

For now, scientists can glean some early clues from known seasonal diseases—including other members of the coronavirus family—that cause common colds every winter.

Becoming seasonal

Though there is no definitive answer as to why some viruses have a seasonal circulation pattern and others don’t, several factors help many viral threats propagate in the winter months specifically.

Many respiratory viruses, such as the common cold and flu, are more stable at cooler temperatures. That allows them to hang in the air for a longer period of time and last longer on surfaces. (Find out what experts say about whether warming temperatures will slow the coronavirus.)

People are also more susceptible to these viruses when temperatures drop. Cold and dry winter weather causes the lining of the respiratory tract to change, narrowing the upper airways and evaporating the moisture layer lining the lungs’ lower airways. This makes it easier for many respiratory viruses to bind with that lining and enter the body.

Winter also finds people spending more time indoors than they do in the warmer months, leading to a drop in vitamin D levels that can increase susceptibility to disease. Vitamin D boosts the function of macrophages and T-cells, members of the immune system that fight pathogens attempting to enter the body.

Vitamin D also helps reduce inflammation—which, “when excessive, is responsible for much viral disease and contributes to death from COVID,” says Kathryn Hanley, a New Mexico State University biologist who studies climate-dependent viruses such as Zika and dengue. Additionally, a lack of vitamin D can impair lung output and can increase the risk for respiratory diseases including asthma, tuberculosis, and chronic obstructive pulmonary disease.

Why seasonality might matter

Even if COVID-19 cases rise significantly this year as the Southern Hemisphere heads into winter, that alone won’t prove that seasonality is the culprit.

Because some known seasonal viruses have been around for a long time, enough people have developed immunities that researchers can more precisely study how those diseases’ behavior changes over time. Currently, though, everyone is susceptible to this coronavirus. The disease is burning through these so-called naïve populations in what’s known as the pandemic stage. During this phase, tracking seasonality patterns in transmission is almost impossible.

“We’ll need three or four years to understand how this virus will behave,” says Marilda Siqueira, a virologist and head of the Respiratory Viruses and Measles Laboratory at the Oswaldo Cruz Institute in Rio de Janeiro.

Establishing seasonality is important because it could play a role in the immunity people ultimately develop against the virus, and in how an eventual vaccine will work.

Our bodies don’t create long-term antibodies for the flu or common cold viruses in the way that they do for the measles. If the coronavirus proves to be similar to influenza in terms of how our bodies respond, the immunity we acquire after being infected might lessen throughout the year. That means being infected one year wouldn’t stop someone from contracting the coronavirus again the next year. In that case, the coronavirus would require an annual vaccine, if one can be made.

Something we do know for sure is that the novel coronavirus is already showing itself to be more dangerous than its close relatives. The original SARS emerged in 2003 and disappeared relatively quickly; new cases have not been seen since 2004. But SARS didn’t have nearly the transmissibility that the novel coronavirus apparently has, Siqueira says.

The World Health Organization says each person infected with COVID-19 is likely to spread it to two others. And a report published April 7 by disease mathematicians at Los Alamos National Laboratory says that number could be three times as high. (Here’s the blood test that can catch “hidden” coronavirus cases.)

That rapid spread helps explain why the death rate of the new coronavirus exploded relative to its predecessors—and why COVID-19 is on track to be much more lethal than known seasonal respiratory viruses, Hanley says. For now, countries in the south can only brace for a situation they’re sure will get worse.

“We have to prepare,” says the University of São Paulo’s Sayuri Sato, “because the peak is still to come.”

