Posted on by Dr. Francis Collins
It was nearly 10 months ago on January 15 that a traveler returned home to the Seattle area after visiting family in Wuhan, China. A few days later, he started feeling poorly and became the first laboratory-confirmed case of coronavirus disease 2019 (COVID-19) in the United States. The rest is history.
However, new evidence published in the journal Science suggests that this first COVID-19 case on the West Coast didn’t snowball into the current epidemic. Instead, while public health officials in Washington state worked tirelessly and ultimately succeeded in containing its sustained transmission, the novel coronavirus slipped in via another individual about two weeks later, around the beginning of February.
COVID-19 is caused by the novel coronavirus SARS-CoV-2. Last winter, researchers sequenced the genetic material from the SARS-CoV-2 that was isolated from the returned Seattle traveler. While contact tracing didn’t identify any spread of this particular virus, dubbed WA1, questions arose when a genetically similar virus known as WA2 turned up in Washington state. Not long after, WA2-like viruses then appeared in California; British Columbia, Canada; and eventually 3,000 miles away in Connecticut. By mid-March, this WA2 cluster accounted for the vast majority—85 percent—of the cases in Washington state.
But was it possible that the WA2 cluster is a direct descendent of WA1? Did WA1 cause an unnoticed chain of transmission over several weeks, making the Seattle the epicenter of the outbreak in North America?
To answer those questions and others from around the globe, Michael Worobey, University of Arizona, Tucson, and his colleagues drew on multiple sources of information. These included data peretaining to viral genomes, airline passenger flow, and disease incidence in China’s Hubei Province and other places that likely would have influenced the probability that infected travelers were moving the virus around the globe. Based on all the evidence, the researchers simulated the outbreak more than 1,000 times on a computer over a two-month period, beginning on January 15 and assuming the epidemic started with WA1. And, not once did any of their simulated outbreaks match up to the actual genome data.
Those findings suggest to the researchers that the idea WA1 is responsible for all that came later is exceedingly unlikely. The evidence and simulations also appear to rule out the notion that the earliest cases in Washington state entered the United States by way of Canada. A deep dive into the data suggests a more likely scenario is that the outbreak was set off by one or more introductions of genetically similar viruses from China to the West Coast. Though we still don’t know exactly where, the Seattle area is the most likely site given the large number of WA2-like viruses sampled there.
Worobey’s team conducted a second analysis of the outbreak in Europe, and those simulations paint a similar picture to the one in the United States. The researchers conclude that the first known case of COVID-19 in Europe, arriving in Germany on January 20, led to a relatively small number of cases before being stamped out by aggressive testing and contact tracing efforts. That small, early outbreak probably didn’t spark the later one in Northern Italy, which eventually spread to the United States.
Their findings also show that the chain of transmission from China to Italy to New York City sparked outbreaks on the East Coast slightly later in February than those that spread from China directly to Washington state. It confirms that the Seattle outbreak was indeed the first, predating others on the East Coast and in California.
The findings in this report are yet another reminder of the value of integrating genome surveillance together with other sources of data when it comes to understanding, tracking, and containing the spread of COVID-19. They also show that swift and decisive public health measures to contain the virus worked when SARS-CoV-2 first entered the United States and Europe, and can now serve as models of containment.
Since the suffering and death from this pandemic continues in the United States, this historical reconstruction from early in 2020 is one more reminder that all of us have the opportunity and the responsibility to try to limit further spread. Wear your mask when you are outside the home; maintain physical distancing; wash your hands frequently; and don’t congregate indoors, where the risks are greatest. These lessons will enable us to better anticipate, prevent, and respond to additional outbreaks of COVID-19 or any other novel viruses that may arise in the future.
 The emergence of SARS-CoV-2 in Europe and North America. Worobey M, Pekar J, Larsen BB, Nelson MI, Hill V, Joy JB, Rambaut A, Suchard MA, Wertheim JO, Lemey P. Science. 2020 Sep 10:eabc8169 [Epub ahead of print]
Coronavirus (COVID-19) (NIH)
Michael Worobey (University of Arizona, Tucson)
NIH Support: National Institute of Allergy and Infectious Diseases; Fogarty International Center; National Library of Medicine
Posted on by Dr. Francis Collins
The pandemic has already claimed far too many lives in the United States and around the world. Fortunately, as doctors have gained more experience in treating coronavirus disease 2019 (COVID-19), more people who’ve been hospitalized eventually will recover. This raises an important question: what does recovery look like for them?
Because COVID-19 is still a new condition, there aren’t a lot of data out there yet to answer that question. But a recent study of 55 people recovering from COVID-19 in China offers some early insight into the recovery of lung function . The results make clear that—even in those with a mild-to-moderate infection—the effects of COVID-19 can persist in the lungs for months. In fact, three months after leaving the hospital about 70 percent of those in the study continued to have abnormal lung scans, an indication that the lungs are still damaged and trying to heal.
The findings in EClinicalMedicine come from a team in Henan Province, China, led by Aiguo Xu, The First Affiliated Hospital of Zhengzhou University; Yanfeng Gao, Zhengzhou University; and Hong Luo, Guangshan People’s Hospital. They’d heard about reports of lung abnormalities in patients discharged from the hospital. But it wasn’t clear how long those problems stuck around.
To find out, the researchers enrolled 55 men and women who’d been admitted to the hospital with COVID-19 three months earlier. Some of the participants, whose average age was 48, had other health conditions, such as diabetes or heart disease. But none had any pre-existing lung problems.
Most of the patients had mild or moderate respiratory illness while hospitalized. Only four of the 55 had been classified as severely ill. Fourteen patients required supplemental oxygen while in the hospital, but none needed mechanical ventilation.
Three months after discharge from the hospital, all of the patients were able to return to work. But they continued to have lingering symptoms of COVID-19, including shortness of breath, cough, gastrointestinal problems, headache, or fatigue.
Evidence of this continued trouble also showed up in their lungs. Thirty-nine of the study’s participants had an abnormal result in their computed tomography (CT) lung scan, which creates cross-sectional images of the lungs. Fourteen individuals (1 in 4) also showed reduced lung function in breathing tests.
Interestingly, the researchers found that those who went on to have more lasting lung problems also had elevated levels of D-dimer, a protein fragment that arises when a blood clot dissolves. They suggest that a D-dimer test might help to identify those with COVID-19 who would benefit from pulmonary rehabilitation to rebuild their lung function, even in the absence of severe respiratory symptoms.
This finding also points to the way in which the SARS-CoV-2 virus seems to enhance a tendency toward blood clotting—a problem addressed in our Accelerating COVID-19 Therapeutic Interventions and Vaccines (ACTIV) public-private partnership. The partnership recently initiated a trial of blood thinners. That trial will start out by focusing on newly diagnosed outpatients and hospitalized patients, but will go on to include a component related to convalescence.
Moving forward, it will be important to conduct larger and longer-term studies of COVID-19 recovery in people of diverse backgrounds to continue to learn more about what it means to survive COVID-19. The new findings certainly indicate that for many people who’ve been hospitalized with COVID-19, regaining normal lung function may take a while. As we learn even more about the underlying causes and long-term consequences of this new infectious disease, let’s hope it will soon lead to insights that will help many more COVID-19 long-haulers and their concerned loved ones breathe easier.
 Follow-up study of the pulmonary function and related physiological characteristics of COVID-19 survivors three months after recovery. Zhao YM, Shang YM, Song WB, Li QQ, Xie H, Xu QF, Jia JL, Li LM, Mao HL, Zhou XM, Luo H, Gao YF, Xu AG. EClinicalMedicine.2020 Aug 25:100463
Coronavirus (COVID-19) (NIH)
How the Lungs Work (National Heart, Lung, and Blood Institute/NIH)
Computed Tomography (CT) (National Institute of Biomedical Imaging and Bioengineering/NIH)
Zhengzhou University (Zhengzhou City, Henan Province, China)