Global Economy

6 reasons why coronaviruses are so bad and 1 reason to not panic

In the past two decades, coronaviruses have produced three deadly global epidemics: SARS, MERS and now Covid-19. If you’re wondering what it is about this family of viruses that makes it produce such deadly pathogens — and what about them might hinder their spread — here are a few things you should know.

1. They have a high substitution rate.

Coronaviruses have, like many RNA viruses, a high substitution rate (though the rate is lower than some other viruses that have caused pandemics, like HIV or hepatitis C). This higher substitution rate means that coronaviruses can rapidly exploit situations in which they come into contact with new hosts (i.e., humans).

2. They mutate rapidly.

One reason coronaviruses mutate so rapidly is that they possess the longest genomes of all known RNA viruses. With more sections in their genome, there are more potential errors when the virus copies itself, which increases the production of new strains (which may explain the recent finding that there are likely to be multiple Covid-19 strains).

3. They are highly susceptible to recombination.

One of the ways viral strains emerge is through recombination, which is when multiple viruses interact in the same organism (e.g., humans) during replication. Research predating the emergence of Covid-19 has shown that, of all the many coronavirus strains that are out there, a human coronavirus known as HCoV-HKU1 is among those most highly susceptible to recombination. It is also one of the coronaviruses most closely related to Covid-19, along with SARS and MERS: all are members of the subset of betacoronaviruses.

4. They replicate in multiple species

Coronaviruses are also exceptionally adaptive and able to replicate in different species. Some viruses, like smallpox, can only infect one species. Coronaviruses can infect — at minimum — humans, bats, pigs, cattle, mice, chickens, civet cats, raccoon dogs, ferret badgers and camels, meaning they have what epidemiologists call “broad host range.” This increases their spread across environments and makes them a lot harder to contain.

5. They love bats.

While scientists suspect that Covid-19 may have initially jumped from bats to humans, bats seem to be uniquely able to harbor many viruses that cause serious human disease: Ebola, Marburg, Rabies, Hendra and Nipah. We can now add Covid-19 to that list. As recently as 2017, a research study that tested bats in Kenya identified several novel coronaviruses that had genomic sequences closely related to human coronaviruses. Why does this matter? This was a one-off research experiment and yet it showed that novel coronaviruses are constantly being discovered in bats.

6. They’ve been around (and evolving) for a long time.

Finally, molecular clock analysis is a technique that uses the mutation rate of viruses to determine when separate strains branched off from common ancestors. When an analysis was done on one of the four known human coronavirus (HCoV-229E, which causes the common cold), scientists discovered that it has been present in the human population for centuries. They were even able to estimate the specific year that it emerged: 1053 AD, which is when it likely branched off from a viral ancestor to become its own strain.

7. They’re heavier than other viruses.

And, finally, the good news. While Covid-19 spreads through the air on respiratory droplets, there is one fact limiting how far the virus can travel: its weight. Coronaviruses are physically larger and heavier than other known respiratory viruses. So while Covid-19 infects hosts via mucus droplets, its infectious range is lower relative to other viruses because its mass limits how far it can travel before succumbing to gravity. Case in point, coronaviruses can only travel about one to two meters, less than seven feet, before they start falling to the ground. Compare that to much more infectious viruses like measles or chickenpox, both of which are much lighter and able to remain airborne on tiny dust particles.


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