When a new disease emerges — SARS, Ebola, COVID-19 — we very rapidly go from total ignorance to knowing quite a lot. A virus or bacteria comes out of nowhere, people get sick and die, and suddenly we have the bug’s whole genome. Research articles on symptoms and therapies, some of them useful, flood the internet. We feel well armed for a swift response.
But the more we learn, the more we discover how little we really know.
Nine months after rumours of a SARS-like pneumonia began to leak out of Wuhan, we now know the SARS-CoV-2 virus seems able to attack almost anywhere in the body, not just the lungs. Some of the attacks are rare but truly horrible, but the worst may be the attacks that don’t stop when the virus is gone.
Doctors call these attacks “sequelae,” and they can be trivial or lifelong chronic disabilities. After the West African Ebola outbreak, researchers found many survivors suffered from eye inflammation, headache, fatigue, muscle pain, joint pain and memory loss. Ebola virus was still in some men’s semen 40 months after they’d recovered.
Similarly, some COVID-19 survivors may have lifelong souvenirs of their experience. Such survivors call the problem “long COVID,” and call themselves “long-haulers.”
Invading any organ
Long COVID reflects the virus’s ability to invade almost any organ, not just the lungs. Early on in the pandemic, the SARS-CoV-2 virus that causes the disease showed it could attack the nervous system: many patients reported they’d lost their senses of taste and smell. The virus can also trigger myocarditis, an inflammation of the heart that causes almost half of all heart transplants in the U.S.
It soon became clear that SARS-CoV-2 can attack not only the heart, but the liver, brain and kidneys. A recent report out of India describes something out of a zombie movie: acute hemorrhagic necrotizing encephalitis, in which the virus effectively destroys the victim’s brain.
Some of these effects kill their victims very quickly. Others, like myocarditis, may take years to make themselves known.
But long COVID seems to emerge very early and then persist. Ed Yong, science writer with the Atlantic, describes a typical long-hauler. “When we spoke on day 150, she was on her fifth month of gastrointestinal problems and severe morning nausea,” he wrote. “She still has extreme fatigue, bulging veins, excessive bruising, an erratic heartbeat, short-term memory loss, gynecological problems, sensitivity to light and sounds and brain fog.”
Clearly, the SARS-CoV-2 virus seems able to attack some people through many different organs. It will be hard to remedy such effects, and far easier to prevent them in the first place — which means knowing their specific causes.
Researchers suspected the answer might be a frequent threat in other diseases like influenza: the cytokine storm. This is a severe over-reaction by the body’s immune system, using small proteins called cytokines. While trying to destroy a perceived invader, the cytokines turn on ordinary cells — something like a police force that begins shooting citizens while restoring law and order.
But that’s a deceptively simple definition of a very complex biochemical response, and it doesn’t seem to apply to long-haulers.
Another inflammatory agent, however, may be responsible for at least some long-COVID effects: bradykinin. It’s a protein that tends to lower blood pressure, and it’s used in treating hypertension and heart failure. It also allows veins to leak fluids into very small blood vessels called capillaries.
In July, American researchers published an article in eLife suggesting that SARS-CoV-2 could induce a “bradykinin storm” that could actually let the virus flood into organs throughout the body. Another article explained this hypothesis in non-technical language. A bradykinin storm doesn’t just release the virus into new territory; it produces a substance that can fill the lungs. As the lead author of the eLife study put it, “It’s like trying to breathe through Jell-O.”
A bradykinin storm could also penetrate the blood-brain barrier, enabling the virus to destroy the victim’s brain — or at least to inflict enough damage to create “brain fog” in survivors. It could also explain neurological symptoms like the loss of taste and smell and “COVID toes” — inflamed toes that resemble chilblains.
Bradykinin’s role is still a hypothesis. But if further research supports it as the virus’s key to flooding the body, then we can develop drugs to reduce bradykinin production and confine the virus. That in turn could help reduce the number of long-haulers.
In the meantime, we have thousands of long-haulers who have struggled for months to recover, and who may struggle for years. Canada has so far recorded about 135,000 COVID-19 cases, 9,000 of them fatal. If even one per cent of the survivors are long-haulers, that’s perhaps 1,200 Canadians with ongoing health issues.
Even asymptomatic cases may find themselves experiencing long-term COVID symptoms, posing another problem for the health-care system.
But the biggest problem may be the public desire to get over the pandemic and forget about it, and to forget about the long-haulers as well.
Somehow we will have to get it through our heads that there is no “short COVID” — it’s not going away anytime soon. For the foreseeable future, we are all long-haulers.