Both coronaviruses, which include the viruses that cause the common cold, as well as the viruses that cause the seasonal flus, are known to flare up in winter and fade away by summer. Will we be so lucky with COVID-19, the coronavirus that is causing a global pandemic?

Many are hoping this will be the case, pointing to previous flus and coronavirus diseases that seem to favor a certain range of temperature and humidity. They infer that the diseases will not tolerate changes in temperature and humidity.

One paper (in preprint stage, before peer review and publication) supports a seasonal demise of COVID-19, which is being community spread in cool and dry weather but not so much in more extreme cold, heat and high humidity. That is what happened with SARS, caused by the virus most similar to the COVID-19 virus, according to researchers from Portugal’s University of Évora and the University of Helsinki.

Temperatures from November 2018-March 2019. Black circles represent areas with more than 6 deaths (all of which occurred in the same temperature range) as of 3/5/3019. (Image courtesy of Climate Reanalyzer.)

Another paper, by Mohammad Sajadi, MD, from the Institute of Human Virology, University of Maryland School of Medicine, confirms that the community spread is occurring mostly in a narrow ribbon of similar temperatures, roughly along the 30-50 N latitude, which also have similar relative humidity (47-79%). Both studies suggest that as temperatures change with the seasons, the community spread will decrease—or even stop—in the afflicted areas.

Harvard professor, Dr. Marc Lipsitch, says that the idea that COVID-19 virus will stop in summer is mostly wishful thinking. “While we may expect modest declines in the contagiousness of SARS-CoV-2 [the virus responsible for the COVID-19 disease] in warmer, wetter weather and perhaps with the closing of schools in temperate regions of the Northern Hemisphere,” said Lipsitch. “It is not reasonable to expect these declines alone to slow transmission enough to make a big dent.”

SARS, caused by the coronavirus most similar to SARS-CoV-2, did not die out because of the temperature change, according to Lipsitch. It did so because of the Chinese government’s stringent health interventions, including finding sick people and isolating them. When Toronto lifted its precautions after the initial surge, this caused a resurgence of the virus, said Lipsitch. The cold virus, even though it is a corona virus, should not be compared to SARS-CoV-2. There’s simply no evidence to indicate that it will act the same way and go away with the cold weather, according to Lipsitch.

Flus don’t always behave according to the season, especially when they first surface. In fact, a pandemic flu of 2009 started in April (not the flu season), took a break in summer (suggesting a link to children who were not in school), and then resurged in the fall—behavior that suggests more of a link to whether children attended school, rather than seasonal fluctuation in temperature and humidity.

In his own preprint paper, Lipsitch concludes that temperature and humidity changes will not necessarily lead to decline in COVID-19. We just don’t know enough to support this claim, and it would be dangerous to stop our screenings and health interventions and just wait for summer.

Most research has focused on the epidemiological spread of the virus, such as person to person. However, work by a University of Utah team has just been fast-tracked by the National Science Foundation to find how the virus particle itself reacts to changes in temperature and humidity.

Michael Vershinin and Saveez Saffarian, researchers from the University of Utah’s Center for Cell and Genome Science in the College of Science, a multidisciplinary group of physicists, chemists and biologists, will be subjecting the SARS-CoV-2 virus to different environments, such as the high summer temperatures and air-conditioned offices, hoping it will fall apart.

“Coronavirus spreads similarly to the influenza virus—as small mucus droplets are suspended in the air. The predominate idea is that viruses lose infectivity because the particles lose structural integrity,” said Saffarian. “The physics of how the droplets evolve in different temperature and humidity conditions affect how infectious it is.”

But rather than testing the deadly virus, the researchers will be literally growing the outside of the virus—its protein-based protective sheath—without the genome so it will be rendered safe and incapable of infecting anyone and replicating itself. This “synthetic coronavirus particle” will essentially be a very small empty bag—and just about as dangerous.

To make the bag, the researchers found the genes responsible for the structural integrity of the virus in the fully sequenced SARS-CoV-2 genome published earlier this year. They are synthesizing the genes in living cells and letting their proteins form the bags that will be used for the study.

To probe the synthetic coronavirus particles to look for signs of damage from a change of environment means working on a nanometer scale (10-9 m), which the University of Utah’s Physics and Astronomy department claims it has decades of experience doing. The researchers will be using an optical tweezer—a laser light beam so fine that it can manipulate atoms.

“It’s often compared with the tractor beam from ‘Star Trek.’ You just use light to reach in and apply force to manipulate things,” said Vershinin.