Is there a link between viral infection and ALS?
- Researchers have identified a specific type of mouse (CC023 strain) that responds to a viral infection in a way similar to humans with amyotrophic lateral sclerosis (ALS), providing a new animal model for studying the disease.
- The study found that the initial viral infection triggers an immune reaction, lesions, and signs of illness, which persists even after the virus is cleared, leading to permanent muscle wasting and ALS-like symptoms in the CC023 mice.
- Four key findings were identified: early nerve damage within two weeks of infection, muscle loss over time, similarities with human ALS symptoms, and an immune response that stops once the virus is cleared.
- The study suggests that genetics play a significant role in susceptibility to viral infections leading to ALS-like disease, providing new insights into the various types of damage caused by viral infections to the spinal cord and its nerves and muscles.
- The CC023 strain offers a unique test track for scientists to identify early warning signs for ALS through biomarkers that appear after infection, potentially leading to testing and new treatments for sporadic ALS, which makes up over 90% of cases.
Researchers have made a potentially game-changing discovery about the development of devastating motor neuron diseases like amyotrophic lateral sclerosis.
The team identified a specific type of mouse—the CC023 strain—that responds to a viral infection in a way that looks remarkably similar to humans with amyotrophic lateral sclerosis (ALS).
“This is exciting because this is the first animal model that affirms the long-standing theory that a virus can trigger permanent neurological damage or disease—like ALS—long after the infection itself occurred,” says Candice Brinkmeyer-Langford, a neurogenerative disease expert with the Texas A&M University School of Public Health.
The CC023 strain provides a unique “test track” for scientists to identify early warning signs for ALS through the biomarkers that appear after infection, she says. In addition, it could lead to testing and new treatments, especially for sporadic ALS, which makes up more than 90% of cases and is not hereditary.
For its study in the Journal of Neuropathology & Experimental Neurology, the team used Theiler’s murine encephalomyelitis virus (TMEV) to infect five strains of genetically diverse animal models. They then assessed how the unique DNA of the different strains affected their responses to the virus during acute, subacute, and chronic phases of infection.
The researchers tracked changes over time and between the different mice strains using five methods:
- Comparing spinal cord inflammation between infected and healthy mice at different times.
- Comparing levels of inflammation among the five mouse strains.
- Determining if higher levels of inflammation were directly linked to more paralysis and other severe physical symptoms.
- Measuring the amount of virus present.
- Testing whether higher amounts of the virus led to higher levels of spinal cord inflammation.
There were four key findings:
- Early damage. Within the first two weeks, all mouse strains showed nerve damage in the lumbar spine. Some strains showed signs of illness as early as four days after infection.
- Muscle loss. Over the long-term phase of the illness, the virus was eliminated from the spinal cord, but the CC023 mice experienced permanent muscle wasting.
- ALS similarities. The CC023 mice showed physical symptoms and lesions very similar to those seen in humans with ALS.
- Immune response. While the immune cells of the mice were very active early on to fight the virus, this activity stopped once the virus was cleared.
In short, the initial viral infection spread and infected the lumbar spinal cord early on, triggering an immune reaction, lesions, and signs of illness. The virus was cleared over time, but the lesions and clinical symptoms persisted, and in the CC023 strain these signs resembled ALS-like disease.
The bottom line, according to Brinkmeyer-Langford? Genetics matter.
“This study gives us a new way to understand the various types of damage caused by a viral infection to the spinal cord and its nerves and muscles, especially since we now know that the initial viral infection triggers lasting, damaging reaction in susceptible individuals,” she says.
Support for this work came from the National Institute for Neurological Disorders and Stroke, National Institute for Environmental Health Sciences, and a National Science Foundation Graduate Research Fellowship.
Source: Texas A&M University
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