Study: First case of COVID in China may have emerged as early as October 2019

AP Photo/Ng Han Guan

This was news to me when I saw it this morning but a little research reveals that it’s at least the third study to push the timeline on COVID’s emergence back from the winter of 2019 to the fall.

Go figure that an analysis of the virus’s origins would hit harder at a moment when the lab-leak theory is front and center in the public consciousness.

Previous studies have used analysis of different early samples of the virus taken from Wuhan to estimate how long it would have taken those samples to diverge from a common “progenitor” virus. Working backwards, they guesstimated when the progenitor began infecting people. This new study from British and Czech researchers borrows a concept from conservation science that’s typically used to estimate when a species went extinct. Using the dates of early COVID cases found in other countries, the researchers worked backward to find a range of time when the virus started passing among the population in China. They even offered a best guess for the exact date that the first case happened.

A peer-reviewed paper published by researchers from the U.K.’s University of Kent and the Czech Academy of Sciences estimates that the SARS-CoV2 virus first appeared between early October to mid-November 2019.

The scientists came to this conclusion by using the optimal linear estimator method which analysed the interval between the first officially reported case in five countries and compared that with the date those cases actually originated.

The study suggests that November 17, 2019, is the most likely date for the virus’ emergence in China and adds that it had probably already spread globally by January 2020—before China began locking down the city of Wuhan.

A genomic analysis published last May also pegged the likely emergence of COVID as having happened between October 6 and December 11, 2019. Another study that appeared in March of this year used molecular dating tools and epidemiological simulations to determine that the virus may have begun circulating in Wuhan as early as mid-October. “Regional newspaper reports suggest COVID-19 diagnoses in Hubei date back to at least November 17, 2019,” researchers noted — the exact data targeted by today’s conservation-science analysis.

What’s interesting about the October/November time frame? Well, October 2019 happens to be the month when there *may* have been a mysterious shutdown at the Wuhan Institute of Virology based on cell-phone data from the location. October 2019 was also when the city hosted the Wuhan Military World Games, attended by 9,000 athletes from around the world — some of whom became mysteriously sick afterward. According to Josh Rogin, members of Congress are now eyeing the games as a possible early superspreader event for COVID-19, one which may have quickly seeded the virus around the world.

And November 2019 was, of course, the month when three employees at the Wuhan Institute of Virology allegedly sought “hospital care” of some sort, which may or may not have been due to infection by SARS-CoV-2.

If you’re looking for evidence to support the lab-leak theory, in other words, an October/November timeline can work for you. On the other hand, the earlier the virus is thought to have originated, the more time it would have had to travel from some other part of China to Wuhan. One virologist made the point on Twitter a few days ago that just because HIV was first detected in Los Angeles obviously doesn’t mean the virus made the jump from animals to humans there. If SARS-CoV-2 or its progenitor really did arise in October 2019, it could have made the jump to some miner in a cave somewhere across the country, then passed to one of his family members, then passed across other people until it infected someone who was en route to Wuhan in December.

Here’s a provocative detail from yet another new study that was published this week, though:

Another study by Australian scientists, published on Thursday in the Scientific Reports journal, used genomic data to show SARS-CoV-2 binds to human receptors far more easily than other species, suggesting it was already adapted to humans when it first emerged.

It said it was possible there was another unidentified animal with even stronger affinity that served as an intermediary species, but the hypothesis that it leaked from the lab could not be ruled out.

Robert Redfield, Trump’s CDC chief, made that point recently in explaining why he believes the virus leaked from a lab. Other respiratory viruses that have made the jump from animals to humans in recent memory, like MERS and SARS 1.0, didn’t spread super-efficiently infecting the planet in a short period of time. SARS-CoV-2 seems surprisingly well suited to infect human beings. Was that a fluke of evolution in the wild? Or is there a more sinister explanation?

We don’t need a sinister explanation necessarily. It turns out bat viruses in the wild are quite good at binding to human cells. No intermediate animal host required:

Dr. Shi’s scientific work was dependent on collecting and analyzing hundreds of bat samples. And it was her work that showed the dangers associated with this endeavor. The 2013 paper by Dr. Shi, Dr. Daszak and others demonstrated that a live bat coronavirus from a Yunnan sample could bind to human lung cell receptors, showing that “intermediate hosts may not be necessary for direct human infection.” That controversial 2015 experiment co-authored by a group of researchers that included Dr. Baric and Dr. Shi was carried out after they had found another bat coronavirus they suspected could infect humans, but it was difficult to cultivate. They then created that chimeric one using its spike. They showed that it, too, could infect human airway cells directly.

I’m eager to hear people who know what they’re talking about weigh in on the Australian study. Do the findings suggest that SARS-CoV-2 was even better suited to infect humans than we’d expect from a bat virus in the wild? How commonly do viruses found in the wild bind more easily to our receptors than to those in other animals?