GIC Long Covid writeupFebruary 8, 2022
One could not be blamed for dreading a recent Global Interdependence Center webinar on long covid, which is coming forward as one of the most concerning and underrecognized aspects of the pandemic. But, as is often the case when science and motivation come together, it was, instead, reassuring to see the work being done to tie together and unravel the complex syndrome.
Even-voiced Bill Kennedy, GIC’s president, opened the program, thanking David Kotok, one of the first to recognize the importance of long covid, for funding the health-care series that is threading together long covid’s effects on science, medical research, public health policy, labor markets, and the insurance industry, as well as implications for fiscal and monetary policy and for geopolitics. The series, in partnership with the Solve Long Covid Initiative, will continue throughout 2022, and we’ll cover each installment. This one is on the science itself.
In his remarks, Oved Amitay, President of Solve M.E. (myalgic encephalomyelitis, also known as chronic fatigue syndrome), noted that his organization recognized and was set to embrace Covid long-haulers as early as April 2020, making their own research available to others at the time, and citing Dr. Fauci’s statement that it is “extraordinary” how people have developed a post viral syndrome that is very strikingly similar to ME/CFS. The symptoms have been defined only more recently.
In her whirlwind presentation, microbiologist Dr. Amy Proal, whose expertise is in the molecular mechanisms by which pathogens modulate and impact human gene expression, pointed out that although long covid is often framed as novel and mysterious, infection associated chronic disease is a well-recognized phenomenon; many studies have connected long-term debilitating effects to Ebola, Dengue, Epstein-Barr, as well as herpes and other enteroviruses. Her teams also pulled, early on, their research to contribute to the understanding of long covid.
Dr Proal highlighted seven ways long covid can get its start, none mutually exclusive. We’re touching on those here, and highly recommend you take a look at the presentation. It’s just an hour long.
The first is the relatively straightforward organ injury from acute covid, the second the possibility that the patient has not completely cleared the virus, and it lingers in a low-level tissue reservoir where, importantly, it cannot be detected by blood tests, but can throw the body out of balance.
It’s always encouraging to see ongoing progress in research advancing the importance of a healthy biome, whether within our own bodies, or within habitat ecologies, where a new still controversial science is looking at the connections between degraded habitats and development of pathogens that can jump species. As of this writing, a zoonotic jump is still considered the most likely origin of the current pandemic, and scientists had warned for decades that the reservoirs of corona viruses in bats and other mammals were a “time bomb.”
Proal’s third proposition gets into that kind of thinking. Weaving together key trends in the immune-metabolism research community, she noted one of her teams identified 54,118 candidate viral species in the human gut, 92% of which had not been identified before that study, leading her to stress that she cannot underscore strongly enough how impossible it is to study any chronic conditions without taking the activity of the trillions of microorganisms that inhabit our bodies into account. Acute covid can reactivate dormant viruses, or bacteria and parasites—one study found that 67% of long covid patients had reactivated Epstein-Barr viruses compared to just 10% of the control group. And many of the microorganisms that are kept in check under homeostasis have the ability to change, in states of imbalance, their gene expressions to become “virulent pathogens,” that can drive “severe disease.”
There is evidence that vagus nerve to brain stem signaling could also produce long-covid symptoms. Sensing ongoing infection or other imbalances, the vagus nerve could send pro-inflammatory signals to the dorsal stem, bringing on pain, nausea and other symptoms, even if the syndrome in different patients were caused by different drivers, including the type of cell infected. Someone asked Dr. Proal why women are more likely to be affected by long covid, which touched on her graduate work on how the receptors that control hormonal signaling also control components of the immune system. Women’s systems show more fluctuation driven by cycles and pregnancy, and finding patterns between core relationships is a promising line of research. (We’ll need policies to address that disparity as well.)
Although long covid is a definite, “who ordered this?” moment, the use of new information by our research teams is inspiring. And it’s all tied together. Just as infections hiding in organs cannot be detected in blood tests, many of the pollutants running in our streams clump together, thereby evading identification by fixed-point sampling. That makes it also an “only connect” moment.
— Philippa Dunne & Doug Henwood
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Please click here to view the replay of this Executive Briefing.
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