The novel coronavirus can stow away in your throat without you knowing it, and every time you cough you’re broadsiding the people around you with the virus. To stay healthy and contain SARS-CoV-2, stay home and keep your distance.
Population-wide efforts to control coronavirus might not be so straightforward, however. The coronavirus is a clever, elusive, and tough little pathogen that could defy normal vaccines.
Those are two of the main takeaways from an important new study by a team of 18 scientists in Germany.
Working in two separate laboratories, the scientists carefully studied the spread of SARS-CoV-2 in the bodies of nine patients, taking daily measurements in order to understand each phase of the infection.
The team completed its study in early March and, published its findings in the journal Nature this month. “Active virus-replication in the upper respiratory tract puts the prospects of COVID-19 containment in perspective,” the scientists wrote.
Close observers of coronavirus studies hailed the German team’s work. There’s “huge news” in the Nature paper, David Ostrov, a professor in the Department of Pathology, Immunology and Laboratory Medicine at the University of Florida College of Medicine, told The Daily Beast.
Some of the news is good.
SARS-CoV-2 starts replicating in the throat, not the lungs. For that reason, a simple throat swab is enough to test for the virus. There’s probably no need for an intrusive, unpleasant nasal swab.
The virus mostly spreads from people coughing on each other. It’s a lot less likely that you’ll catch the coronavirus by touching the same touchpad or toilet handle as an infected person.
It’s probably safe for a hospital to release a COVID-19 patient 10 days after they start showing symptoms.
There’s bad news in the German study, too.
The antibodies our bodies produce in response to COVID-19 infection don’t actually destroy this virus. In that way, it is a lot like HIV.
That has implications for the high-stakes global effort to develop vaccines and other treatments.
Besides containing important takeaways for doctors, scientists, and the public, the German study also tells a story. One that helps to make sense of the pandemic.
Peter Kolchinsky, a virologist and biotech investor, summed up the Nature paper on Twitter. The study, he wrote, “reveals a remarkable trick SARS-CoV-2 learned that makes it nastier than the first SARS,” which killed nearly 800 people during an outbreak in 2003.
Viruses access our cells by interfacing with particular proteins. Once inside, they hijack our cells’ own mechanisms in order to make copies of themselves. When that happens, our bodies sometimes panic, mobilizing a powerful immune response that can go too far… and make us sick or even kill us.
It turns out, SARS-CoV-2 prefers a spiky protein called ACE2.
“Think of it as a particular doorknob that the virus knows how to turn,” Kolchinsky explained in his summary of the German paper.
We’ve got a lot of those ACE2 proteins in our throats, which are great places for a virus to hide out, replicate, and get ready to spread.
From the throat, the pathogen can spread inward to the lungs, where it becomes a lot more dangerous to the host. And with each cough it projects outward into the world. All without us even knowing it’s there.
Beating the coronavirus pandemic requires people to block the virus’ preferred method of travel—coughs—before they even know they have it. “There’s an evil genius to viruses that never ceases to amaze me,” Kolchinsky wrote.
Ostrov for his part focused on the German team’s findings on antibodies, which our bodies produce via a process called “seroconversion.”
“When aligned to viral load courses, it seems there is no abrupt virus elimination at the time of seroconversion,” the scientists wrote. “Rather, seroconversion early in week two coincides with a slow but steady decline of sputum viral load.”
“This means that the antibodies are not effective at clearing the virus,” Ostrov told The Daily Beast. “This is relevant when thinking about viruses and vaccines. HIV also stimulates production of antibodies that fail to clear the virus, as do many other viruses, such as hepatitis virus C.”
“People have tried and failed to generate vaccines against such viruses, so we should not be overconfident that a vaccine strategy will work,” Ostrov added.
That doesn’t mean we don’t try to develop a coronavirus vaccine. Vaccines might end up working.
If they don’t, scientists might consider switching up their strategy. Instead of leaning on vaccines to inoculate us, doctors could treat SARS-CoV-2 infections like they do HIV. With a cocktail of drugs that manages, but does not eliminate, the infection.