Plate Nº 53 · recorded September 30, 2026
Health & Medicine ResearchReported finding
Common Viruses May Speed Up ALS, McMaster Study Finds
McMaster researchers found that flu and COVID-19 triggered lasting spinal inflammation in ALS models, speeding decline—but antivirals and anti-inflammatories slowed it.
By Marcus Bennett4 min read726 words
In brief
- In animal models of ALS, a single influenza A or SARS-CoV-2 infection significantly accelerated motor decline, with inflammation persisting in the spinal cord after the virus cleared.
- Neither virus infects neurons; the damage appears to come from gliosis, an inflammatory immune response in the nervous system already known to play a role in ALS.
- Treating infections with antivirals or suppressing gliosis with anti-inflammatories significantly reduced the rate of ALS progression in the study.
A single bout of influenza or COVID-19 may be enough to accelerate the progression of amyotrophic lateral sclerosis (ALS), according to a new study from McMaster University published in Nature Communications.
The findings point to something unexpected: the viruses themselves may not be the main problem. Instead, the study suggests that the immune response these infections trigger—a process called gliosis, in which immune cells in the nervous system become inflamed and form scar tissue—lingers in the spinal cord long after the body has cleared the virus. That lingering inflammation appears to speed up the disease.
ALS, commonly known as Lou Gehrig's disease, is the most common motor neuron disease, affecting roughly one in 300 Canadians. It progressively damages the nerve cells that control movement, eventually causing severe weakness, paralysis and death. There is no known cure, which is why researchers are focused on identifying the environmental factors that influence when the disease begins and how quickly it worsens.
What the researchers did
Scientists in the lab of Matthew Miller, a professor of biochemistry and biomedical sciences at McMaster, monitored animal models of ALS after infecting them with either influenza A virus or SARS-CoV-2, the virus that causes COVID-19. They compared these animals with a group of uninfected ones. The infected animals showed a much more rapid decline in motor function.
While researchers have long observed a link between viral infections and neurodegenerative diseases, it has remained unclear how infections from very different viruses could all appear to raise risk. Much of the earlier work was epidemiological—tracking patterns in populations—without probing the underlying biology.
"A lot of the previous work in this area has been epidemiological in nature, without much focus on the molecular mechanisms that actually underpin the connection between infections and ALS," says Imran Ahmed, a master's student in Miller's lab and co-first author of the paper along with lab alumni Art Marzok and Jonathan Mapletoft. "What makes our study unique is that we did take a mechanistic approach—we explored why this connection might exist."
Inflammation that outlasts the virus
A striking feature of the results is that neither influenza A nor SARS-CoV-2 actually infects neurons. Even so, both viruses left lasting changes in the nervous system.
In the animal models, the infections triggered gliosis—an inflammatory response from immune cells in the nervous system—that stayed elevated in the spinal cord even after the virus was gone. Gliosis is already known to play an important role in ALS. The new findings suggest that infection can amplify this process, helping to accelerate the disease.
For Marzok, who completed both a Ph.D. and a postdoctoral fellowship in Miller's lab, one of the most striking details is that a single infection could prompt this response.
"In our preclinical models, just one viral infection was enough to significantly accelerate ALS progression, even after the infection itself had resolved," says Marzok. "These findings strongly suggest that viral infections—and the inflammatory responses that they trigger—may fundamentally influence the course of the disease."
Treatments made a difference
The study also tested two interventions. The researchers treated infections with antiviral drugs and suppressed gliosis with anti-inflammatories. In both cases, they saw a significant reduction in the rate of ALS progression.
Miller, who is scientific director of the Michael G. DeGroote Institute for Infectious Disease Research and executive director of NexusHealth, says the results point toward possible ways to delay onset and slow progression in the absence of a cure.
"Developing better vaccines and antiviral therapies—and improving the public's trust in them—could have health benefits that we don't fully appreciate," says Miller. "Our work here suggests that preventing or limiting common infections could at the same time protect your nervous system from the damage that accelerates ALS."
Reasons for caution
The results come from animal models, so they do not yet prove that the same mechanism drives ALS progression in humans. Whether preventing or promptly treating common infections would meaningfully alter the disease course in patients remains an open question that will require clinical research.
Still, the study offers a concrete biological explanation for a connection that researchers have observed for years, and it identifies two potential intervention points—the virus and the inflammation—that future therapies might target.
via Medical Xpress (Source)
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