"The worst enemy of the coronavirus is spring": what we know about how heat and humidity affect outbreaks of COVID-19

In the fight against the coronavirus, we have an ace up our sleeves: time works in our favor. And I speak of time in its two usual meanings, the chronological and the atmospheric. Researchers and health authorities are convinced that SARS-Cov-2 will be affected by ambient heat and humidity.

The same Fernando Simón, the director of the Center for Health Alerts and Emergencies of the Ministry of Health, said a few days ago that “the virus with high temperature and lower humidity will be more fragile and it will be like a flu that stops transmitting in spring-summer. If so, by spring it will decrease and may be undetectable. " But how can we know this? What leads us to think that this will be the case with a virus that we have known for so little time?

Heat and humidity: weak points of the SARS-2

The first thing is its molecular structure. As Alberto García-Salido explains, COVID-19, like most animal viruses, has a viral envelope. This envelope is a lipid bilayer that, coming from infected cells, facilitates the entry of the virus. This envelope does not sit well with high temperatures and, as far as we know from other coronaviruses, heat accelerates its inactivation.

This can be verified in the laboratory, but also in other epidemics. In the most similar case that we have to the current crisis (that of the SARS of 2003), the outbreak began in November, reached its peak in May and, in practice, disappeared with the arrival of summer in the northern hemisphere. However, as we have repeated many times, what we know about other coronaviruses does not have to be fulfilled in this one, but it does give us a good frame of reference that until now has been very useful to us.

On the other hand, there are many more factors that influence the spread of infectious-contagious diseases. Many of them of a social and cultural nature. The classic example is that, in winter, people tend to be more in closed spaces where interpersonal contact is closer and vitiated environments cause the viral load of the air to increase. Others, on the other hand, are meteorological: the heat causes the mucus and the microflows thanks to which they are transmitted to dehydrate with greater speed.

In short, there are good reasons to think that the arrival of heat and the dryness of the environment will be a fundamental factor in order to stop the epidemic. And that is good news. Not only because it will help stop the chains of infections already underway, but also because it offers us a window of opportunity to achieve our goal, to eradicate the disease before it becomes permanently established in humans.

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