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Nicholas Christakis on fighting covid-19 by truly understanding the virus

In an Aug. 10 article in The Economist, NOMIS researcher Nicholas Christakis explains that understanding how the novel coronavirus is different from SARS-CoV-1 is essential for identifying how society can best confront it.

The latest coronavirus is different from past ones, so requires a different response

Nicholas Christakis by Dan Williams (Photo: The Economist)

SEVEN VARIETIES of coronavirus infect humans: four give us the sniffles; one causes a deadly disease smouldering in the Middle East since 2012; and two erupted into full-on pandemics. The first caused SARS and it petered out quickly. The other causes covid-19 and it has hobbled the global economy. Why the difference?

It is not only a matter of the public-health response or governmental incompetence (though that has certainly made things worse). It also has to do with the underlying epidemiology of the pathogen, which we are coming to appreciate, after little more than a half-year of experience. Viewing covid-19 through the lens of SARS can lead to flawed responses. Understanding how the novel coronavirus is different is essential for identifying how society can best confront it.

SARS, caused by the virus known as SARS-CoV-1, appeared in 2002 and spread to 30 countries. But it infected only 8,422 people and killed just 916 before being declared “contained” by the World Health Organisation eight months later. On the other hand, the virus behind covid-19, SARS-CoV-2, has infected more than 18m people and killed more than 700,000 so far.

On the surface, the pathogens have several aspects in common, beyond belonging to the same family of coronaviruses (and having genetic sequences that are 79% identical). Both emerged in China in late autumn and were noticed in a place where wild animals and people were in close proximity: a seafood market in Guangdong for SARS, and a similar market in Wuhan for covid-19. Both produced respiratory ailments and could be lethal. Their transmissibility or “reproduction number” (the now famous R0) was also roughly the same, with each victim infecting about three other people, on average.

But that is where similarities end. The virus behind SARS had intrinsic qualities that made it harder to spread and easier to control, compared to the one behind covid-19, which has overwhelmed the world. This is because of their respective fatality rates, symptoms, infectious periods and a nuance in their reproduction number. Consider these features in turn, for they explain why covid-19’s virus has been so destructive—and how we can best fight it.

First, fatalities. One way that epidemiologists quantify lethality is the case fatality rate, which is the probability a person will die if they come to medical attention. SARS’s case fatality rate was around 11%. Covid-19’s is estimated to be in the range of 0.5-1.2%, making it one-tenth as deadly as SARS. This makes it harder to control because there are more walking wounded. SARS did not spread as far because it was, paradoxically, too deadly. (This also helps explain why the Ebola epidemics that can rapidly claim a terrifying 80-90% of infected people in some African outbreaks eventually wane.)

Continue reading this Economist article


NOMIS Researchers

Sterling Professor of Social and Natural Science, Internal Medicine & Biomedical Engineering
Yale University
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