Six months after the novel coronavirus first leaped from animals to people in Wuhan, China, and three months after the virus began spreading across the United States, scientists are finally beginning to understand the overall shape of the pandemic.
Drawing samples from tens of thousands of COVID-19 patients and decoding the samples’ genomes, scientists are making so-called “phylogenetic” maps of the pandemic over time. The maps help researchers start to answer some important questions.
How did SARS-CoV-2 spread in the absence of travel bans and stay-at-home orders? How did transmission patterns change once countries, regions and cities finally began shutting down? What effect have the shut-downs had on the virus’ mutation? The answers could help inform ongoing efforts by governments, hospitals and businesses to contain the virus and treat its victims. They could also help public-health officials write the playbook for the next global pandemic response. Assuming, that is, that people actually want to learn from the current crisis.
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“We now have enough SARS-CoV-2 genomic data from different states to make some broad conclusions about how the covid-19 epidemic has unfolded in the U.S.,” Trevor Bedford, a University of Washington epidemiologist tweeted.
Bedford’s analysis, combined with the efforts of a team of researchers led by Cambridge University geneticist Peter Forster, reveals a global map of viral transmissions over time.
After bouncing around China for a few weeks starting in December 2019, the novel coronavirus more or less simultaneously spread to Europe and other parts of East Asia. By early March, there were three fairly distinct major strains of the pathogen, Forster’s team concluded after studying 160 samples from COVID-19 patients all over the world.
The researchers called the strains A, B, and C.
“The A and C types are found in significant proportions outside East Asia, that is, in Europeans and Americans,” Forster’s team explained in a March 30 article. “In contrast, the B type is the most common type in East Asia, and its ancestral genome appears not to have spread outside East Asia without first mutating into derived B types.”
SARS-CoV-2 strains leaped more or less directly from China to Los Angeles and Seattle in late January or early February, according to one of Bedford’s phylogenetic maps.
A few weeks later the virus traveled to New York City after a lengthy and devastating stop-over in Italy, another one of Bedford’s maps reveals.
By then it was mid-March, and countries and communities all over the world—even in the late-acting United States—were shutting down. That’s when the pandemic’s main dynamic changed. Rather than quickly jumping from travel hub to travel hub in the form of a handful of major strains, SARS-CoV-2 settled down in self-isolating towns and cities… and mutated.
Under lockdown, the pathogen began spreading inside of communities rather than between them. Family members infecting each other while under quarantine. Co-workers getting each other sick on the job.
To be clear, it’s not that community transmission wasn’t happening before. It was. And it’s not that lockdowns haven’t helped slow the overall rate of infections, buying time for hospitals and local governments to hone their responses. The lockdowns have worked— and have saved countless lives.
But in all but halting the coronavirus’ long-distance leaps, social distancing measures made community spread more prominent in comparison.
Community spread introduced an important new dynamic. Bottled up in towns and cities with many thousands of potential hosts all in close proximity, SARS-CoV-2 apparently started mutating into many different strains. “The original Wuhan strain was already in the country, doing well and popping up new subtypes all across the country,” Guido Grimm, a widely published phylogeneticist, told The Daily Beast.
A couple months later, scientists have identified the major subtypes. “There seem to be anything up to a dozen distinct genetic variants in the USA,” David Morrison, a biologist at Uppsala University in Sweden, told The Daily Beast.
And these distinct variants of the virus could eventually end up being more dangerous than the early variants.
In early May, a team of scientists in Los Alamos, New Mexico, claimed it had found “evidence of recombination between locally circulating strains.” One result, the team claimed, was the emergence of a particular mutation of SARS-CoV-2 that has become dominant in some American cities because it spreads more easily.
“These findings have important implications for SARS-CoV-2 transmission, pathogenesis and immune interventions,” the scientists wrote.
To be clear, the Los Alamos study hasn’t been peer-reviewed yet and some scientists have questioned the researchers’ conclusions. But Morrison for one thinks they might be onto something. “Their work may be a bit premature,” Morrison told The Daily Beast, “but their general point is quite valid.”
That point—that the coronavirus has begun evolving into local strains —should inform the response to the pandemic moving forward, Morrison said. “Our response may well have to be different for different mutations, because most responses target the genome in some way. Finding a general therapeutic response is hard, and usually takes years, for precisely this reason.”
It’s not hard to imagine different cities developing different therapies for their local strain of SARS-CoV-2. But before they can tailor their treatment strategies, doctors first need to know exactly which strain or strains they’re dealing with.
That demands more and faster testing. “Genomic sequencing of all infections routinely in the clinic would help,” Alice McHardy, a researcher in computational biology at the Helmholtz Centre for Infection Research in Germany, told the Daily Beast.
Such sequencing is “cheap nowadays,” McHardy said.
Phylogenetic mapping has helped us understand the novel coronavirus pandemic to a degree that past public health officials might have envied. But that doesn’t mean that we’re going to preserve this knowledge and apply it to the next pandemic.
To stop a virus like SARS-CoV-2, it’s important to lock down fast. And once you’ve locked down, you have to test exhaustively in order to keep up with the fast pace of mutations.
But if history is any indication, we’re likely to forget these lessons.
Humanity didn’t learn all that much from the far deadlier flu pandemic of 1918, Morrison pointed out. Why would we learn anything from the current crisis? “I am sorry to say that the same lessons are re-iterated by the professionals with every pandemic, and they fall on deaf ears every time.”