Though they’ve saved lives and helped control, and even eradicate, disease for centuries, vaccines have never had an easy or straight narrative. In 1717, Lady Mary Wortley Montagu, the wife of the British ambassador to Turkey, witnessed her first variolation in Constantinople. A precursor to vaccination, the process involved inserting a thread into the pustule of a person infected with a mild case of smallpox, and then inserting that saturated thread into a small cut in the arm of a healthy person, where it was left to soak for twenty-four hours. The motivation behind the experimental procedure was simple: everyone seemed to know that if a person survived smallpox, they never became infected with it again. So why not try to induce a mild, survivable case to ward off a more serious one? At the time, this method of protecting against smallpox—a disease that could both kill and permanently disfigure—was common in the Middle East and Asia, but not in Lady Montagu’s home continent of Europe. As someone who’d survived but been gravely scarred by the disease, she vowed to have her children undergo variolation. When it worked, she spread the gospel upon her return to England. The apparently miraculous procedure was, however, met with plenty of skepticism, and it was initially carried out only on prisoners, who were offered freedom if they survived. Eventually, the method gained advocates across the Western world. George Washington used it to inoculate his entire army. Catherine the Great tried it, and the Princess of Wales inoculated her daughters. The controversy stuck, though: variolation was expensive, and it risked both killing its recipients and further spreading the disease.
Still, the process undoubtedly inspired Edward Jenner, who is frequently dubbed the “father of vaccination.” Working as a rural doctor in England, Jenner noticed that milkmaids infected with cowpox, a mild illness, also seemed to gain immunity to smallpox. Though he wasn’t the first to notice the seeming coincidence, he was the first to document it and to gather data to confirm it. And, in 1796 he convinced his gardener to let him experiment on the man’s eight-year-old son. (Eighteenth-century England may have been the peak of new science, but it was evidently not so great on the ethics front.) Jenner first gave the boy the cowpox virus, and then smallpox. He called his new process a “vaccination,” drawing from the Latin word vaccinus, meaning “from cows,” and thus naming the method after the black-and-white spotted animals that had made it possible. The smallpox vaccine came with less risk than variolation, and Jenner quickly gained high-profile converts, including Pope Pius VII and Napoleon, as well as high-profile controversy.
Indeed, the birth of vaccines arrived with a twin: the birth of the anti-vaccination movement. In part, Jenner did some of the damage himself. He refused, even in the face of good evidence, to admit his vaccine did not offer lifelong immunity. (Today, it’s believed the smallpox vaccine lasts up to twenty years before a person has to be revaccinated.) But opposition also came in the form of libertarianism: people resented the apparent intruding powers of the state, under what they saw as the guise of public health measures—call it, perhaps, the great, great, great, great grandparent to the current anti-mask movement. Others feared it violated God and nature to put something from a cow inside a human. As Frank M. Snowden wrote in Epidemics and Society, cartoons depicting vaccine recipients as hapless horn-sprouting monsters began to rise in popularity. One doctor stoked the hysteria, added Snowden, by saying women who took the vaccine would wander into fields and embark on sexual relations with bulls. Nonetheless, Jenner’s smallpox vaccine marched on over the next two centuries and, in 1980, the WHO declared victory over the virus. Thanks to a concerted public health effort and vaccines themselves, naturally occurring smallpox was wiped from the earth.
But the anti-vaccination movement persisted. Less than two decades after smallpox was eliminated, British surgeon Andrew Wakefield published a since-debunked article in the Lancet that linked the measles, mumps, and rubella vaccine to autism-spectrum disorders. It didn’t seem to matter that biological signs of autism are readily visible in utero, or that it was later discovered that he’d knowingly fabricated the medical histories of his subjects, or even that he accepted six hundred thousand dollars from a law firm planning to sue vaccine manufacturers. As Joshua S. Loomis sharply noted in Epidemics, “Suddenly, everyone was an infectious disease expert because they had read a secondhand account of a study on a blog or website.” It was, as Loomis put it, “an explosion of ignorance.” Once rare, measle outbreaks began reoccurring, and have continued to do so. Whooping cough was under control for decades, something that is no longer true. The scrutiny and misinformation campaign surrounding the human papillomavirus (HPV) vaccine has allowed the virus to stick around. The more resistance there is to the idea of preventable disease, the more opportunity said diseases have to evolve. The anti-vaccine movement has the same potential to damage efforts against COVID-19. In October 2020, for example, Nature Medicine released a survey of people in nineteen countries that showed only 71.5 per cent said they would be very or somewhat likely to take a COVID-19 vaccine. The rest said they would hesitate or outright refuse. It’s just enough for herd immunity in Canada, but it’s still distressing—especially since a December 2020 survey of Canadians showed only 48 per cent would immediately roll up their sleeves for a shot. (It was, at least, a welcome 8 per cent rise from the month before.) As those such as Kelvin and Elnicki do their parts, it will still be up to the rest of us to do ours.
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If vaccines are the nuclear bomb in the fight against COVID-19, antivirals are the infantry. Unfortunately, though, viral illnesses are notoriously harder to treat than bacterial infections. In fact, after the discovery of penicillin in 1945, it took nearly another forty years for the first antiviral drug to be licensed. As noted earlier, pathogenic bacteria are largely free-living, single-celled organisms. That means antibiotics can target bacteria cells within the body while leaving our own cells unharmed. Viruses, on the other hand, are gifted hijackers that use our own cells to replicate themselves. Because of this, it’s difficult to stop their reproduction without harming the host. While certain antibiotics can treat a wide variety of bacterial infections, antivirals are usually limited to a single virus, or a virus group. The first licensed antiviral, aciclovir, was introduced in the 1970s and treated herpesvirus infections, including cold sores and chickenpox. Like a virus, aciclovir is tricky, camouflaging itself as a nucleoside, the building block of DNA. Essentially, it terminates viral DNA replication and spares uninfected host cells. The crew of HIV antiviral drugs, taken together, is another example of a working, established drug therapy. The flu can also be treated with antivirals that inhibit the virus and block its entry into host cells. And, as Canada registered record-breaking case counts and the U.S. watched its own case count climb unabated in October, the latter country approved the first COVID-19 drug. Remdesivir is an antiviral that can cut recovery times by five days. It was a big breakthrough, but it wasn’t the only one.
Throughout the end of 2019 and early 2020, immunologist Eleanor Fish was, as usual, travelling abroad. At each conference or academic institution, she shared the same message. “The twentieth century was the century of bacteria, and then along came antibiotics,” she told me. “The twenty-first century is going to be one of viral infections.” So, she’d asked the gathered experts, how are we going to handle this? How are we going to prepare ourselves? Closer to home, the U of T professor and scientist at the Toronto General Hospital Research Institute would share another, additional warning: Canada is a lightning rod for viral outbreaks. Our wonderfully diverse population means that people will arrive at our border from all around the world. They will cross it, in both directions, by plane, boat, train, car, and some of them, sometimes, will bring a virus with them. It doesn’t matter where the outbreak originates, added Fish. When it stops moving, the chances are it will end up here, where it will spread. Because of all this, she thinks it is a lost cause to keep developing pathogen-specific antivirals. “You’re always playing ca
tch-up,” she explained. A virus will travel, mutate, adapt, develop resistant strains—all of it often outpacing human speed. As an example, she pointed to Tamiflu, or oseltamivir, which many countries, including Canada, stockpiled in 2009 to fight the H1N1 swine flu pandemic. Canada recorded its first case on April 26, 2009, and its first aseltamivir-resistant case scant weeks later on July 21, 2009. It is not inconceivable that remdesivir could meet a similar fate. Which is why Fish argues it’s time to stop making pathogen-specific drugs and try something else: interferons.
Interferons are a set of proteins that already occur naturally within our bodies. Our immune system cells secrete them in response to viruses and other threats. Discovered in 1957, interferons can be grouped into several classes that, together, help regulate the body’s immune system response. They can, as the name suggests, interfere with viral proliferation, enhance innate or acquired immune system responses, and also respond to cancerous growth. When it comes to viruses like SARS-CoV-2, an infected cell may release interferons, stimulating nearby cells into entering an antiviral state. In other words, interferons won’t kill a virus directly, but they will trigger a defence response in other cells, preventing the virus from replicating within them. This will, in turn, stem infection—sort of like turning each healthy cell into a battle fortress. Their use as a pharmaceutical product is not new. Since the 1980s, they’ve already been used to treat everything from Ebola to multiple sclerosis, to varying, and not always remarkable, effect. Fish herself has been studying their applications for decades. She has long believed that they do have a “wow factor” but that scientists have also missed interferons’ true calling: as the perfect first responders in a global pandemic.
In December 2019, as news of the emerging novel coronavirus trickled out of Wuhan, Fish contacted colleagues in China who immediately set up an exploratory study using interferons to treat virus patients at a hospital in Wuhan. She was glad, but not exactly surprised, to discover the interferon treatment worked. Between January 16 and February 20, doctors administered interferon treatment to a total of seventy-seven people at the Union Hospital, Tongji Medical College at the Huazhong University of Science and Technology. The patients presented with a moderate case of COVID-19, and although they had been admitted into the intensive care unit, they did not require supplemental oxygen; it was early on into their possible disease progression. Researchers defined viral clearance as two consecutive negative tests at least twenty-four hours apart. Results were significant. Interferon treatment had accelerated viral clearance by approximately seven days. That’s even faster than remdesivir, noted Fish. The treatment also reduced inflammatory markers of the disease. “Interferons are a no-brainer,” she added.
Fish and her colleagues’ study was published in May 2020 in Frontiers in Immunology. The publication had an oddly dual outcome: she became incredibly busy and optimistic, and also incredibly frustrated. When we spoke months later in early August, she joked that when she “allows” her iPhone to give her notifications, she will receive constant emails and calls from around the globe, from 7:30 a.m. until 11 p.m. She has helped researchers worldwide map out clinical trials, craft journal publications, edit research papers, and learn about interferon treatment. She has been asked, and has sometimes agreed, to join the scientific advisory boards of several pharmaceutical companies. She’s given dozens of media interviews, everywhere. In short, she’s made herself available around the clock. But even as she’s seen interest in interferons explode, she’s also seen a blanket of apathy.
If interferons were on, say, a dating app for antivirals, they’d have a lot going for them to make a person swipe right: they’re already FDA approved, they have three decades of clinical experience, and they can work on a wide number of viruses—all of which also makes them an economically sound choice. Unfortunately, they have also not been very effective in their main use to date, which is against chronic virus infections. In that context, they work just “okay” and can have side effects that are “really quite unpleasant,” said Fish. (It may be worth noting here that Fish is British by birth, and has the exact dry humour you might expect from a British scientist.) She knows that’s why, even in the face of increasingly positive evidence, some scientists have been hesitant to throw them at another challenge. Luckily, that reticence had already started to shift when we spoke, thanks in large part to her persistence. Early on in the pandemic, she had, for example, shared her findings with the United States’ Dr. Anthony Fauci, who, as Fish put it, “passed it on to his team, where it died a nice death.” She noted, though, that it had since been resurrected, and that a randomized control trial was finally underway, too, which would only add to the growing body of evidence. And Fish thought fondly of her colleagues around the world who emailed her with their own disbelief as researchers scrambled to develop an antiviral, overlooking the one that already existed, and worked.
“Until there are organizations independent of Eleanor Fish who say, ‘Yes, this looks promising,’ ” she noted, “This is going to be an uphill battle that continues.” Still, Fish is used to proving people wrong. In 2014, she ran an interferon trial in Guinea to treat Ebola; the virus has more than a 60 per cent fatality rate in the country. Despite established protocol and recommendations, she refused to make it a randomized control trial; she believed the interferons would work and did not want to “randomize people to death.” In the end, she convinced everybody there was enough historical data to provide an accurate contrast between those who received the treatment and those who didn’t. And that contrast was stark: 67 per cent of the interferon-treated patients were still alive three weeks after infection, while only 19 per cent of those who received the standard care survived at day twenty-one. The study was so successful, she’s now helping local health authorities develop an interferon clinic. Beneath all the frustration, COVID-19 offers a chance to prove naysayers wrong again. In the process, Fish won’t only be helping us make it more safely through this pandemic—she’ll be showing us how to better survive the next one.
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Recovery is a complex thing. It goes deeper than vaccines and antivirals, further than containing SARS-CoV-2. It encapsulates the economy, human rights, housing, social resources, health care, what we demand from our governments, and what we’ll no longer tolerate. Past pandemics spurred revolution and religion, squashed civilizations, and forked the course of history again and again and again. This pandemic is equally unlikely to fade quietly, returning the planet to 2019 in a great time-travel machine. Certainly, many people hope that it doesn’t. Paulette Senior, the president and CEO of the Canadian Women’s Foundation, is one of them. Of course, like all of us, she wants COVID-19 to stop. But as 2020 raged on, she also began to see the pandemic’s possibility as a Great Reset. Watching how quickly society pivoted, all over the world, gave her hope. What she saw is that when all of our lives are at risk, humanity is capable of doing better. When it matters—and so many things still matter, from stopping domestic violence to fighting anti-Black racism to creating income equality—we can change. “All the old excuses of how difficult it would be to do this and that went out the window,” said Senior. “And instead we could let in some fresh air.”
Senior has spent much of her life tackling systemic barriers, particularly for women and girls. She’s worked in social services, focusing on Toronto’s most underserved neighbourhoods. She’s managed shelters and employment programs and was the CEO of YWCA Canada for more than a decade. Her experiences when she was a young child as a newcomer from Jamaica to Canada also exposed her to her own set of systemic barriers. Which is to say, she has spent more than thirty years pushing for change and then the pandemic reaffirmed to her that such change can happen. We can transform in a heartbeat. It isn’t about what’s possible or impossible any longer, she told me. It’s about: What kind of world are we committed to building? And, what kind of choices are we making when it comes to those whom the pande
mic has most disastrously affected? If the pandemic has shown us that everything can come undone in an instant, it’s also shown us that everything can be remade. We’ve seen unprecedented death and struggle, but we’ve also seen unprecedented kindness, leadership, support, and breathtaking innovation. We’ve seen that we’re not stuck with what we have. So when we rebuild, argued Senior, why not rebuild something better—something that is in the best interest of all of us, and not just some? She has many ideas about what that could include: universal child care; inclusive, robust education that tells history from a more truthful perspective; a policing system that protects everybody and doesn’t cost billions; committed, non-divisive politicians; “When we decide that we, as human beings, are the priority,” she added, “everything else will follow from that decision.”
Under that hopeful, adamant perspective—that we can build better—the Canadian Women’s Foundation has released a series of research papers on building a better normal. Other women’s organizations have joined them in their vision for a new Canada. For example, Senior’s former organization, YWCA Canada, and the Institute for Gender and the Economy at the University of Toronto’s Rotman School of Management jointly released a feminist economic recovery plan in July 2020. In it, they outlined eight “non-negotiable” steps the country should take to generate future prosperity, for everybody. Like Senior, the report’s authors also saw hope in the broad range of people across Canada who, perhaps for the first time ever, realized things needed to change. To them, it looked like a necessary, and also encouraging, paradigm shift. They also recognized what many others, from PSWs to community leaders, had already stressed: COVID-19 alone isn’t what broke us. “It took a pandemic for the country to see what was already broken,” wrote the authors. “We cannot ignore the historical context that has created the unstable foundation for the harms we are seeing play out in this current crisis.”
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