text: 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.