Study shows immune responses to flu and COVID-19 trigger lasting inflammation in the spine, hastening onset/progression of amyotrophic lateral sclerosis (ALS).
RT’s Three Key Takeaways:
- Viral Infection Impact: Preclinical research indicates that common respiratory infections, such as influenza A and COVID-19, can hasten the onset and accelerate the progression of amyotrophic lateral sclerosis (ALS).
- Persistent Spinal Inflammation: Researchers found that respiratory infections trigger elevated gliosis in the spinal cord that persists even after the pathogen has cleared, intensifying neurodegenerative damage.
- Therapeutic Potential: Interventions using antiviral drugs or anti-inflammatory agents to suppress gliosis significantly slowed ALS disease progression in preclinical models.
Common viral infections, including influenza and COVID-19, may accelerate the onset and progression of amyotrophic lateral sclerosis (ALS), according to a study published in Nature Communications.
While viral illnesses have historically been linked to neurodegenerative disorders, researchers have sought to determine how distinct respiratory pathogens produce similar adverse neurological outcomes. According to the study, the accelerated decline in motor function is driven by the host immune response rather than direct viral infection of neurons.
“ALS is a debilitating and incurable disease, so it’s critical that we improve our understanding of the common environmental factors that can hasten its onset and accelerate its progression,” said Matthew Miller, a professor of biochemistry and biomedical sciences at McMaster and principal investigator on the study, in a news release. “Understanding what triggers or accelerates the disease could illuminate new strategies for slowing or even stopping it.”
Mechanisms Driving Accelerated Decline
ALS is the most prevalent motor neuron disease, progressively destroying nerve cells responsible for voluntary muscle movement and eventually resulting in paralysis and death, according to background information cited in the study. In Canada, the condition affects approximately one in 300 individuals.
To examine how respiratory pathogens influence the condition, investigators evaluated animal models of ALS infected with either influenza A virus or SARS-CoV-2. Compared with uninfected controls, the infected models demonstrated a significantly faster decline in motor function.
The authors noted that previous investigations into infections and neurodegeneration were largely observational, whereas this study focused directly on the underlying biological pathway.
“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,” said Imran Ahmed, a master’s student in Miller’s laboratory and study co-first author. “What makes our study unique is that we did take a mechanistic approach — we explored why this connection might exist.”
Lasting Immune Response in the Spinal Cord
The research team reported that common respiratory viruses leaving lasting impacts on the central nervous system trigger gliosis, an inflammatory response mounted by immune cells in the nervous system. In the animal models, elevated gliosis in the spinal cord persisted even after the host cleared the respiratory infection.
“In our pre-clinical models, just one viral infection was enough to significantly accelerate ALS progression, even after the infection itself had resolved,” said Art Marzok, study co-first author and former postdoctoral fellow in Miller’s laboratory. “These findings strongly suggest that viral infections — and the inflammatory responses that they trigger — may fundamentally influence the course of the disease.”
Implications for Clinical Management and Prevention
Beyond identifying the inflammatory pathway, the researchers tested targeted interventions in preclinical models. When infections were treated promptly with antiviral therapeutics, or when gliosis was suppressed using anti-inflammatory drugs, the models exhibited a significant reduction in the rate of ALS progression.
These outcomes suggest that limiting viral illness and controlling downstream neuroinflammation could offer viable therapeutic strategies for patients managing motor neuron disorders, according to the research team.
“Developing better vaccines and antiviral therapies — and improving the public’s trust in them — could have health benefits that we don’t fully appreciate,” said Miller, scientific director of the Michael G. DeGroote Institute for Infectious Disease Research. “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.”
