If there is one thing most of us have learned about the coronavirus itself, we know it is covered with spikes.
In news broadcasts about the COVID-19 crisis, that gray Styrofoam ball dotted with red spikes has become an unofficial logo of the pandemic.
We even see the spikes as they appear — with artificial coloring — in photos from powerful electron microscopes. They ring the body of the virus like jewels in a crown, hence the name of this microbial family — coronavirus.
Biologically speaking, those spikes are critically important. They are literally the point of contact that our own vulnerable lung cells have with the virus, SARS-CoV-2. Like a key cut for a specific lock, the spike slides neatly into the matching sites of receptors found on cells that line the airways of our lungs. Once secured, this connection allows the entire ball-shaped virus to slip into the cell. Inside, it makes thousands of copies of itself. And the potentially lethal infection has begun.
Learn more about SARS-CoV-2 and pandemics in this companion story, A short primer on coronavirus biology.
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Yet this spike has qualities that make it different from other feared contagions like HIV and influenza, giving scientists a possible route to an effective vaccine or cure. Genetically, it is relatively stable compared to surface proteins on other viruses, and that makes it less of a moving target for antibodies or drugs designed to block it.
“That’s good news for slowing resistance to antivirals. It’s good news for vaccine development,” said Dr. Michael Emerman, a virologist at Fred Hutchinson Cancer Research Center in Seattle.
A researcher at Fred Hutch and the University of Washington, Emerman is a leading expert on how pandemic viruses like influenza, HIV and SARS cross from animals to humans. It is thought each of those viruses, on their evolutionary journeys, jumped from another species: Influenza from birds to humans, HIV from chimpanzees, SARS — and its close cousin SARS-CoV-2, most likely from bats.
Influenza and HIV are known for surface structures made of proteins and sugars that rapidly change their shape. Attempts to block HIV with a vaccine have failed for three decades because of that virus’ ability to hide from the human immune system, including from those tiny proteins called antibodies that are raised naturally against HIV’s surface. Influenza viruses are shape shifters as well, because they evolve new surface structures against antibodies from vaccines. That forces vaccine makers to reformulate flu shots against different strains every few years.
Coronaviruses are genetically more stable because they carry within them a mechanism for correcting errors that naturally occur through mutation of their genetic code. The genomes of HIV, flu, and coronavirus are all made of RNA, which is less stable and more prone to error than the DNA that stores our own genetic information. All three viruses mutate because they rely on RNA, but coronaviruses do so more slowly.
Therefore, researchers have reason to hope that if they can come up with a treatment or vaccine that locks onto those signature spikes of coronavirus, it is less likely to make a quick escape and is more likely to be controlled.
One thing that is different about the arrival of SARS-CoV-2 from pandemics of the past is that researchers are now equipped with tools that have enabled them, within weeks of the discovery of the virus, to sequence its genome and model the protein structure of the spikes. Using cryo-electron microscopes — which give scientists astoundingly accurate images of the spike — we already know the knobbly terrain of its surfaces and likely spots on it for antibodies or drugs to dock and possibly disable it.
Fred Hutch scientists — and researchers throughout the world — are feverishly working to find antibodies that naturally attach the SARS-CoV-2 spike, gumming up its ability to enter lung cells so easily. These tiny proteins could be produced in the lab and used as drugs to block the virus, and they might serve as the basis for a new vaccine or blood tests that show prior exposure to the virus. They could prove to be critical in the fight against COVID-19.
Sabin Russell is a staff writer at Fred Hutchinson Cancer Research Center. For two decades he covered medical science, global health and health care economics for the San Francisco Chronicle, and wrote extensively about infectious diseases, including HIV/AIDS. He was a Knight Science Journalism Fellow at MIT, and a freelance writer for the New York Times and Health Affairs. Reach him at firstname.lastname@example.org.
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