Women of the Pandemic

by Lauren McKeon

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  As the night slipped in, Dr. Alyson Kelvin put down her glass of wine and closed her book. Ready for sleep, she reached to turn off her light and, like so many of us, decided instead to check her email one last time. At 11:59 p.m. on December 30, she had received an alert from the Program for Monitoring Emerging Diseases, or ProMED-mail, a free email service with over eighty thousand subscribers—the same service from which Allen received her January 3 alert. Kelvin, who is a virologist at Dalhousie University and the IWK Health Centre in Halifax, jokingly calls it “a social network for infectious disease researchers.” Started in 1994, and run by the International Society for Infectious Diseases, the global listserv has been the first to report on SARS, MERS, Ebola, and Zika outbreaks. Because the open-access service also tracks potential toxins and emerging diseases in animals and plants, however, not every notice is so dire. Kelvin points to one email from Russia about a fungus outbreak in radishes, dryly noting why she doesn’t read every alert. But this one—featuring a broken English translation from a Chinese news site, emailed under the subject line “Undiagnosed pneumonia, China”—caught her attention.

  ProMED editors warned that the social media chatter surrounding the virus sounded eerily similar to the early reports that swirled around SARS. “Returning to the rumor mill,” read the email, archly noting an absence of concrete information, “the discussion of this outbreak involves an ‘atypical pneumonia.’ ” The estimated case count was “apparently” twenty-seven, a rapid-fire, perverse connect-the-dots that happened in a matter of days, weeks at most. Kelvin was alarmed: if so many people were hospitalized, the pathogen must be severe. How many others were sick but not at the hospital? She wasn’t ready to wave the pandemic flag, but she did want to know more. Kelvin forwarded the email to her father, David, who is also an infectious-disease researcher at Dalhousie and who had established a lab in the Guangdong province of China in 2003 after the SARS outbreak. His response the next day was brief: “Interesting.” And, it was. The word dangerous would come later.

  Though Kelvin had hoped for more, the new pneumonia-like virus wasn’t yet on her father’s radar—it was hardly on anyone’s radar in Canada during the first party-hangover days of 2020. But Kelvin couldn’t let it go, especially as more people were hospitalized. She reasoned that they couldn’t all have gone to the wet market in Wuhan and interacted with the same species, even if that’s where the virus originated. It seemed much more likely that, despite assurances otherwise, the unknown virus could spread through human-to-human contact. If that were true, she worried the global consequences of a spillover could be catastrophic. Her lab at Dalhousie was not equipped to study such deadly pathogens, so she reached out to the University of Saskatchewan’s Vaccine and Infectious Disease Organization—International Vaccine Centre. More commonly known as VIDO-InterVac, the sprawling lab is a world leader in vaccine research and development. She asked them, “Do you have the virus? Can you get it?”

  The new virus wasn’t yet a blaring-red warning for VIDO, either. But Kelvin pushed, and researchers there acquiesced. Before Canada even had its first case, the lab had their permits in place to work on the virus if—when—it arrived. In the meantime, Kelvin began writing research grants to fund what she saw as the inevitable work she would undertake on SARS-CoV-2. It was mid-January, and she kept having to rewrite the sentence charting the global case count. Every time the numbers went up, she’d reopen the document, delete the number, type in a new one. January 23: 570. January 30: 7,818. January 31: 9,800. Delete, replace, delete, replace, do it again. As she wrote, she also planned her trip to VIDO, ticking off each step in the complicated clearing process. Background check, done. Supplies gathered, done. Eventually, the only thing left to do was wait. And then came the call from Public Health Ontario: Sunnybrook had the country’s first case, and Mubareka had agreed to share her sample with VIDO. On February 24, Kelvin, her graduate student, Magen Francis, and a technician got on a plane.

  If early 2020 felt like a storm to Mubareka, to Kelvin it felt like walking down a long, pitch-dark hallway, the only light shining straight at your feet. You could guess your way forward but never know every direction, what was beyond your own private circle of dusk, or how far you had left to go. It wasn’t impossible for her to imagine a pandemic; she knew as she packed her suitcase in February that March would look different. People would not be hollering, shoulder-to-shoulder, in crowded stadiums. They would likely not be jet-setting on spring vacations. But as for how bad it would get, and how far it would spread—she had no idea. The unpredictability terrified her, especially as a mother of two young daughters. Initially, she followed her plan to stay at VIDO for three and a half weeks, studying the virus and beginning work on a vaccine, and to then return home. By that time, the world had plunged into the dark hallway alongside her.

  The WHO declared COVID-19 a worldwide pandemic on March 11, not long before Kelvin’s flight back to Halifax. She stayed home for a week before hopping back on the plane. “I realized even before I left that I needed to come back,” she said. “I needed to continue.” So she checked into a hotel with a small kitchenette, hung up her clothes, discovered her favourite takeout. Just four more weeks, she thought. Another month and then she’d have done enough research into how the virus transmitted. She’d have answered her questions about why men seemed so much more susceptible than women to severe disease symptoms and hospitalizations. She’d know the life cycle of the virus, what it did to the body, and when. And in knowing all that, she’d know how to stop it from taking over a body, infecting its cells, waging war at the molecular level. She’d have done enough to help VIDO develop a vaccine. Except COVID-19 proved remarkably elusive, evading answers, patterns, logic. The first month passed. Then, the second. Then another and another and another.

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  In Canada, there are only a handful of Biosafety Level 3 labs—the classification given to facilities that are equipped to study the world’s most deadly pathogens. Normally, they compete: for research grants, funding, prestige—for the ability to say they did something first or published earlier than everyone else. Scientific discoveries are guarded, progress kept secret. If it were another time, or if Mubareka were another type of scientist, she might have decided to keep Canada’s first COVID-19 sample to herself. Instead, she gave her blessing for every sample she initially collected to be shipped to VIDO, where, because of Kelvin’s early insistence, the lab was already set up to study the virus. When Sunnybrook was ready to begin its own work on the virus in late February, Mubareka made another decision: once her team was successful in isolating SARS-CoV-2, she’d share the virus with any Canadian Level 3 lab that wanted it. Forget competition. If the world were to stand a chance against the swiftly moving pandemic, open science needed to triumph. She wasn’t the only one who thought so. Soon, other scientists were repeating her new mantra. “It’s better to collaborate than to compete,” they said.

  But to collaborate on anything, someone first needed to isolate the virus. Having a clean and endless source of SARS-CoV-2 would allow Canadian scientists to decode the virus’s genetic material, to infect other cells, and to run infinite test models. Without such a supply, it would be impossible to develop any effective medical countermeasures against COVID-19, including antivirals and vaccines. Isolating the virus would be a tricky task, though, and would involve what Mubareka calls “a little old-school virology.” Not only was SARS-CoV-2 new, but science had only recognized the wider coronavirus family itself in the 1960s—to a collective yawn. Scientists largely ignored the bunch of them for decades (even though two of the forty different types are responsible for between 15 and 30 per cent of “common cold” symptoms). They simply weren’t deadly enough to be interesting. That is, until the first SARS-CoV virus emerged in 2003, spreading from a bat to a person to the world, before it largely fizzled out a year later. Even then, when the
close biological copy of SARS-CoV-2 struck, many virologists in Canada were still focused on other, more lethal things—Zika, West Nile, HIV. As Mubareka has said, “We are really starting from scratch.”

  Luckily, a few important traits of SARS-CoV-2 were familiar. Like any other virus, a coronavirus needs a host cell to survive. When an infected person sneezes or coughs, they expel virus-loaded droplets into the air and onto surfaces, giving the virus its chance to propagate. From there, a healthy person may inhale or touch a droplet, ushering the virus into their body and laying out an unintentional welcome mat at their nose and throat. The coronavirus will then hijack the cell’s machinery, creating endless doppelgangers, invading and infecting, typically moving further and further into the respiratory system. Within their core, coronaviruses all have a strand of RNA, similar to DNA in that it contains the genetic information of the virus, including what information it needs to replicate—a sort of Art of War for disease. A lipid-based barrier encapsulates and protects the RNA genome, and also anchors the structural proteins it needs to keep spreading. (Like most fatty things, that barrier breaks down under soap and water, which is why hand-washing works.) Lastly, the crown-like protrusions, called spike, allow the virus to latch on to the body’s cells, cracking their defences like an egg.

  The “old-school virology” Mubareka drew from involved using viral culture to support, and spur, that SARS-CoV-2 growth process. Ironically, to reach the end goal of killing the virus, scientists first had to give it life. This type of virology stretches back decades. In 1933, scientists isolated the influenza A virus using ferrets. In this case, the Sunnybrook team decided to try a non-human primate, landing on the kidney cell of an African green monkey. Known as Vero cells, and first derived in 1962 from a dissected monkey in Japan, they are popular among virologists because of their high susceptibility to, well, nearly everything. Along with Arinjay Banerjee, a post-doctoral research fellow at McMaster who bunked in her spare room to save precious commuting time, Mubareka then began the trial-and-error process of cultivating the virus. After deciding on the culture, she gathered viral swabs from COVID-19 patients and, working with the rest of the team, put each infected swab into a viral transport media. From there, Mubareka would give whatever swab she was working with a little shake, causing the virus to glide off, becoming suspended in the medium. Moving carefully, she’d then take the now virus-laden medium and drop it into a tray of small wells, not unlike Jell-O moulds. Next, she’d rock the mixture gently, allowing the virus to rise to the top of the culture cells. “And then it’s kind of like waiting for a cake,” Mubareka said, laughing—you do nothing for a little bit, but, if you got everything right, the virus will grow.

  On the other hand, a lot can go wrong. If you take a sample from a person’s nose, for example, you might inadvertently scoop up pesky immune factors, impeding the virus’s ability to spawn. Certain bacterial toxins could contaminate your sample. Or, you might have cultivated a different coronavirus entirely. If Mubareka and Banerjee had done any of that, they wouldn’t have known right away. A human cell is about 10,000 nanometres; a coronavirus is 90 nanometres, scant billionths of a metre (and, for that matter, also much smaller than any type of bacteria)—meaning that, even when the human eye has help, without an electron microscope, the virus is more or less invisible. Instead, Mubareka had to rely on seeing the damage. The first time they tried to cultivate the virus, the monkey cells looked “unhappy,” but the team wasn’t convinced it was the destructive work of SARS-CoV-2. So, they decided to try to trick the virus again into doing what it does best: ravaging. And, on the second try, they saw it more clearly. Now, there were holes where the virus had caused cells to disintegrate, called a cytopathic effect—think of it as a punched-out paper snowflake. It was promising, but Mubareka wouldn’t be convinced until a molecular test confirmed the virus’s full genome sequence. She noted, “I’m very conservative with these things.”

  Within a week, the test clinched it. Shortly after, photos from an electronic microscope confirmed it again, showing the virus’s telltale namesake, the corona—Latin for “crown.” On March 13, Sunnybrook announced that its lab had isolated the virus. Mubareka kept her promise and shared virus cultures with any Containment Level 3 lab that wanted them, which, as it turned out, was most of them. The day Sunnybrook announced the isolation, Canada recorded forty-two new cases, and it was only three days into the pandemic. The more virus samples researchers could now isolate, the better. A virus isn’t stagnant. Over time and across geographies, SARS-CoV-2 would likely mutate and evolve, seeking new ways to survive and always, always replicate. Multiple samples and isolates allowed microbiologists to examine and trace its changing nature as it spread, a relentless wave carried on by crowded cities and global travel, a hyper-connected world.

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  When Amy Greer received the ProMED warning at the end of 2019, her mind blinked back a decade to the 2009 H1N1 influenza pandemic. At the time of the virus’ second wave, she had worked for the federal public health agency, supporting the country’s pandemic preparedness and response activities. She remembered building mathematical models, estimating and re-estimating the potential spread of what was commonly called swine flu, after its similarity to influenza viruses found in pigs in North America and Eurasia. Like the strange new coronavirus, the then-new influenza had a unique combination of genes that had never been seen in either humans or animals. The first worldwide case was reported in Mexico on March 18, 2009, and it would go on to kill more than four hundred Canadians. Greer, now a professor at the University of Guelph and a Canada Research Chair in Population Disease Modelling, called a few colleagues whom she worked with on H1N1. She wanted to know if they’d also been following the news out of Wuhan.

  “I don’t know if I’m being paranoid or not,” she told them, laughing, just a little, at the absurdity of what she was about to say. “This might be a complete waste of time.” Hesitation. “But maybe we should dust off our pandemic models.” Her colleagues agreed, and together they started building the necessary code, hoping they wouldn’t have to use it. By late February, Greer started going through her pantry, taking stock. Her husband was startled. “He said, ‘Geez, normally you’re very laid back,’ ” she recalled. “ ‘If you’re telling me we need a quarantine stockpile, then I’m starting to get worried.’ ” So was Greer. They tried to think of everything they might need. She quizzed herself: Do we have batteries for the thermometer? Do we have an extra bottle of children’s Advil? If everything shuts down, are we ready? At work, she asked different questions, formulating distinct scenarios based on the dynamics of the emerging pathogen and then projecting that knowledge forward in time: If we did nothing to mitigate transmission, what would happen a month from now, two, three? What if we retreated, actually did shut down everything, distanced from each other? What if we all wore masks? What would be necessary to slow down transmission?

  Without strict intervention, many possible outcomes showed the same thing: collapse. Epidemiologists and mathematical modellers were still learning about the biology of the virus, but they did know it appeared to be highly transmissible. In scant weeks, the virus had undulated across the globe, spreading through Italy, Iran, and Brazil. It had skulked aboard a cruise ship anchored on a Japanese shoreline, infecting more than six hundred people—at the time, the largest outbreak outside China. Models from different countries, even using slightly different methods, consistently estimated that 60 to 70 per cent of their populations could become infected if the virus were to spread unchecked, without interception by public health. The numbers felt staggering, unfathomable. The air buzzed with the possibility of mass death. It buzzed with denial. Even Greer and her colleagues couldn’t say with certainty what would happen. The new coronavirus was behaving in puzzling ways. Most viruses wreak havoc on the very old and the very young. During the 1918 Spanish flu pandemic, mortality rates were particularly high for children
under age five. Children also suffered more during swine flu. But SARS-CoV-2 barely seemed to infect children at all. Many wondered if kids were actually faring better or if they just hadn’t had the chance to become infected yet.

  As new information trickled through to her via open access research networks, Greer adjusted and updated her models, emailing the findings to her network of government contacts and public health officials. The virus may have been a series of question marks punctuated by even bigger question marks, but she did know that, to slow transmission, people needed to significantly change their day-to-day behaviour. She knew it would be a hard sell. In mid-March, many parts of the country still had zero cases. The virus felt terrifying, but also mythical, a fire-breathing dragon, a Marvel villain, something from over there. She worried politicians would be willing to wait until there were more cases, and then it would be too late to put on the brakes. Hospital intensive care units would be overwhelmed. Ventilator capacities would buckle. She was surprised, and relieved, when immediate, aggressive stay-at-home orders were issued. She also knew that, despite hopes at the time, three weeks wouldn’t be enough. So, when the National Post asked her what it would take to stop thousands of deaths, she answered honestly.

  For centuries, the idea of social distancing and mass lockdowns have figured strongly in public health responses to disease outbreak. During the 1918 Spanish flu, which would be deeply mined for lessons in pandemic management in the months ahead, cities all over the world limited public gatherings and adjusted business practices. Some did so drastically; others, less so. New York City merely staggered its business hours, for instance, with the aim of reducing crowds. It also educated city-dwellers on the dangers of coughing and spitting in public. Other cities shut down everything, including schools, libraries, movie theatres, stadiums, and any other places where people gathered in mass numbers. San Francisco and San Diego required anybody who went out in public to wear a gauze mask. But, just like with COVID-19, timing mattered. Cities that waited weeks to implement measures—even those with the strictest rules—suffered high mortality rates. (Philadelphia had one of the highest in the U.S.; it knowingly held a parade after the virus had started infecting the city.) Other places that acted immediately, such as St. Louis, fared better. So too did cities that refused to lift restrictions as the pandemic peaked. Then, just as now, the dissemination of information also mattered. Some media downplayed the pandemic, encouraging a false sense of safety. And, on top of that, wrote Joshua Loomis in Epidemics: The Impact of Germs and Their Power over Humanity, politicians worldwide couldn’t seem to agree on anything: “This produced unnecessary delays and created confusion in populations who often were getting mixed messages.” Sound familiar?