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For almost a decade, scientists chased 
the source of a deadly new virus

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through China’s tallest mountains 
and most isolated caverns.

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They finally found it here: in the bats 
of Shitou Cave.

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The virus in question was a coronavirus

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that caused an epidemic of severe acute
respiratory syndrome, or SARS, in 2003.

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Coronaviruses are a group of viruses

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covered in little protein spikes that 
look like a crown—or corona in Latin.

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There are hundreds of 
known coronaviruses.

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Seven of them infect humans, and can 
cause disease.

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The coronavirus SARS-CoV causes SARS, 
MERS-CoV causes MERS,

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and SARS-CoV-2 causes the 
disease COVID-19.

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Of the seven human coronaviruses, 
four cause colds,

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mild, highly contagious infections 
of the nose and throat.

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Two infect the lungs, and cause much 
more severe illnesses.

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The seventh, which causes COVID-19, 
has features of each:

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it spreads easily, but can severely 
impact the lungs.

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When an infected person coughs, droplets
containing the virus spray out.

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The virus can infect a new person when
the droplets enter their nose or mouth.

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Coronaviruses transmit best in 
enclosed spaces,

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where people are close together.

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Cold weather keeps their delicate casing
from drying out,

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enabling the virus to survive for longer 
between hosts,

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while UV exposure from sunlight 
may damage it.

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These seasonal variations matter 
more for established viruses.

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But because no one is yet immune 
to a new virus,

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it has so many potential hosts that it
doesn’t need ideal conditions to spread.

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In the body, the protein spikes embed in 
the host’s cells and fuse with them—

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enabling the virus to hijack the host
cell’s machinery

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to replicate its own genes.

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Coronaviruses store their genes on RNA.

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All viruses are either RNA 
viruses or DNA viruses.

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RNA viruses tend to be smaller, 
with fewer genes,

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meaning they infect many hosts and 
replicate quickly in those hosts.

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In general, RNA viruses don’t have 
a proofreading mechanism,

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whereas DNA viruses do.

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So when an RNA virus replicates,

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it’s much more likely to have 
mistakes called mutations.

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Many of these mutations are useless or 
even harmful.

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But some make the virus better suited
for certain environments—

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like a new host species.

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Epidemics often occur when a virus 
jumps from animals to humans.

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This is true of the RNA viruses that 
caused the Ebola, zika,

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and SARS epidemics and the 
COVID-19 pandemic.

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Once in humans, the virus still mutates—

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usually not enough to create a new virus,

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but enough to create variations, 
or strains, of the original one.

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Coronaviruses have a few key differences 
from most RNA viruses.

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They’re some of the largest, meaning 
they have the most genes.

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That creates more opportunity for 
harmful mutations.

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To counteract this risk, coronaviruses 
have a unique feature:

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an enzyme that checks for replication 
errors and corrects mistakes.

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This makes coronaviruses much more 
stable,

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with a slower mutation rate, 
than other RNA viruses.

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While this may sound formidable,

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the slow mutation rate is actually a 
promising sign

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when it comes to disarming them.

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After an infection, our immune systems 
can recognize germs

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and destroy them more quickly if they
infect us again

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so they don’t make us sick.

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But mutations can make a virus less 
recognizable to our immune systems—

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and therefore more difficult to fight off.

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They can also make antiviral drugs 
and vaccines less effective,

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because they’re tailored very 
specifically to a virus.

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That’s why we need a new flu vaccine
every year—

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the influenza virus mutates so quickly 
new strains pop up constantly.

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The slower mutation rate of coronaviruses
means our immune systems,

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drugs, and vaccines might be able to 
recognize them for longer after infection,

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and therefore protect us better.

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Still, we don’t know how long our bodies
remain immune to different coronaviruses.

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There’s never been an approved treatment
or vaccine for a coronavirus.

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We haven’t focused on treating the ones
that cause colds,

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and though scientists began developing
treatments for SARS and MERS,

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the epidemics ended before those 
treatments completed clinical trials.

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As we continue to encroach on other 
animals’ habitats,

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some scientists say a new coronavirus 
jumping to humans is inevitable—

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but if we investigate these unknowns, 
it doesn’t have to be devastating.