The Death Star. The Flowered Planet. The Devil’s Gobstopper.
The coronavirus known as SARS-CoV-2 is, to borrow a phrase from Winston Churchill, a riddle wrapped in a mystery inside an enigma. Scientists have mapped its contours and measured its structures to atomic-level precision. They have come to understand its genetic ancestry with a precision that leaves 23andMe in the dust. They have watched it go to work on human cells in a lab.
But after close to six months among us, this coronavirus continues to startle and confound. Why does it kill some and barely graze others? Will it wane through the summer months and surge come fall? Once we understand its behavior, could it just … change?
We do know that this uninvited guest is an organism that cannot survive long outside a living mammalian host. Once picked up off a counter or drawn in from a bystander’s cough, the virus will seek out cells with structures on their surfaces that it can latch onto.
It will then enter the cell and commandeer its machinery to do what it cannot do on its own: to replicate itself, over and over again.
Governed by a 30,000-base genome coiled up inside its core, the virus will perform that task imperfectly. But it will do it well enough to send millions of copies of itself on to other cells in the lungs, the heart and the gastrointestinal tract.
Eventually, this zombie army will attract the attention of its human host’s immune system. In some people, the response will be swift and effective. Others will fight through weeks of misery and emerge depleted but well.
In an unlucky few, the immune system counterattack will run amok, wreaking havoc on organs not meant to have joined the fight. Death by multi-organ failure can ensue.
We also know this: that everything required for this fateful encounter with human cells is right here, re-created in three-dimensional detail by the biomedical visualization studio Visual Science.
Each of the millions of units that make up the virus seen here is an atom, and colors are used here to distinguish distinct structures from one another. These deeply researched illustrations join a garden of other viral models executed by the firm, including ones for HIV, Ebola and Zika. With a hint of whimsy, they call this collection the “Viral Park Project.”
The SARS-CoV-2 virus is an average-sized virus, bigger than the enterovirus that causes polio and smaller than the herpes simplex virus that causes cold sores and genital herpes. Its diameter is roughly 1,000 times smaller than that of a human hair, and it is one of just seven coronaviruses known to cause illness in humans.
Unlike the snake-like Ebola virus or the egg-shaped H1N1 influenza virus, the form of the coronavirus varies. It is shown here as spherical. Its surface is studded with an average of about 90 spike proteins (in red) that give it its name. “Corona” is Latin for crown.
In the image above, the spike proteins and the virus’ fatty outer membrane (in gray) have been cut away to reveal its core of nucleocapsid proteins (in green). These contain and protect the single strand of 30,000 RNA nucleotides that govern the virus’ structure and function.
At the virus’ core, the genetic code is tightly intertwined with protective proteins that instruct the host cell in viral production and assembly. Among viruses whose genetic material is made of RNA, coronaviruses have the largest genomes. But compared with DNA viruses, coronaviruses are generally smaller, less complex and less accurate in replicating themselves. Each time SARS-CoV-2 replicates, about 30 mutations can be expected to occur.
Membrane proteins are shown here as clusters of pink and purple atoms sitting on the surface of the virus. These are the most abundant of the coronavirus’ protein types, and they’re the only ones that interact with all the others to ensure that the virus is properly assembled and the spike proteins are held in place.
Above and below, the clusters of whitish orbs scattered across the virus’ surface and spikes are glycoproteins, or proteins decorated with sugars. They help the virus to identify and then bind to receptor sites on the cells it seeks out. They also help shield the virus from the immune system by casting a kind of cloud over it. And they prevent coronaviruses from clumping together in ways that would reduce their efficiency.
The five-headed “envelope protein” (in the center here in pale green) is the smallest and most mysterious of the coronavirus’ four major structural proteins. It appears to be crucial to a virus’ ability to invade and take over a host cell. The envelope protein serves as an “ion channel,” pumping sodium and potassium in and out of the cell’s internal compartment to create a favorable environment for the coronavirus’ replication.
When coronaviruses have been altered in a lab to lack these envelope proteins, the resulting viruses have been unable to copy themselves quickly or accurately. Scientists say vaccines to thwart the coronavirus and therapies to treat COVID-19 might focus on disrupting the supply or function of this enigmatic protein.
In the image above, immune system proteins called antibodies are shown orbiting the coronavirus. The protruding spike proteins contain receptor-binding sites called epitopes that antibodies try to locate and plug in a bid to foil the virus’ ability to dock with a cell and hijack its functions.
A vaccine against SARS-CoV-2 would use one of many possible strategies to teach the immune system to recognize the coronavirus. If successful, the lymphocytes of the body’s adaptive immune system would respond by generating so-called neutralizing antibodies that seek and attach to the spike proteins.
Seeing the coronavirus in such intimate detail should inspire awe, both for the courage of scientists who have painstakingly peeled back the virus’ layers in the lab and for the skill of illustrators who have made them so visually compelling.
It’s hard not to feel some respect, too, for the power of a relatively simple microorganism to upend life as we know it.