-We've seen countless depictions of it --
the mysterious novel coronavirus
that has started a global pandemic.
It invades our body on so small a scale
that it's invisible to the human eye.
But even though we can't see it,
what we do know about viruses can provide a way to defeat it.
Humans have an interesting relationship with viruses.
We often think of viruses as foreign invaders,
but viruses are longtime residents of our body --
on our skin, in our intestines and other organs.
Many of these viruses, known as phages,
even protect us from harmful bacteria.
Viruses are so enmeshed with human DNA
that at least 8% of our genes come from ancient viruses.
But it's ambiguous whether viruses are even alive.
They can't reproduce on their own,
so they hijack our cellular equipment
to make copies of themselves.
The coronavirus does this through its corona,
or crown of protein spikes.
The virus uses the shape of these proteins
to gain entry into the cell, like a key in a lock.
And like any clever thief, it disguises itself
by changing the physical appearance of the protein
and masking it with a coat of sugars
to trick our immune system.
When the entrance is unlocked,
the virus is free to deposit its genetic material
and set up shop, replicating itself.
How do we know the novel coronavirus does this?
Well, years of experience with SARS, MERS,
and other coronavirus-related diseases
have given us a head start.
Severe acute respiratory syndrome, or SARS,
is a coronavirus disease that started in China in late 2002.
Similar to COVID-19, SARS infects the respiratory system,
especially the lungs, where the disease is most lethal.
COVID-19 shares almost 80% of its genes with SARS,
which is why this novel coronavirus disease
is officially known as SARS-CoV-2.
10 years after the outbreak of SARS,
another lethal coronavirus disease
spread through the Arabian peninsula --
MERS, or Middle East respiratory syndrome --
proved to be just as deadly,
so much so that transmission of both diseases
burned out after several months of containment.
COVID-19, SARS, and MERS are all zoonotic,
meaning the virus originated in animals
before it came to humans.
And when the novel coronavirus took that jump,
it targeted the same entry points
that the SARS coronavirus had --
proteins called angiotensin-converting enzyme 2,
or ACE-2 for short.
These enzymes are found on cells in our throat,
nose, kidneys, and lungs.
Normally, they help regulate blood pressure for the body.
Coronaviruses turn them into a back door.
The spread of the coronavirus
between the upper respiratory area,
where the virus is most transmissible,
and the lungs, where it is most dangerous,
may be why COVID-19 is potentially more contagious
than MERS and SARS and also deadlier than the flu.
Research has shown COVID-19 to be at least
10 times more likely to bind to ACE-2 receptors than SARS.
The tighter the connection,
the easier it is for the virus to break into a cell
and replicate before moving on to its next host.
Virus copying doesn't always go as planned,
and coding mistakes make for mutations,
some that end up destroying the virus.
Luckily for us, this coronavirus is not mutating quickly,
which means that any treatment developed
will be more effective for longer.
We're still in the dark on many aspects
of how COVID-19 operates.
Sure, it's a microscopic war with an unknown enemy,
but at least the territory is not completely uncharted.