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Magdalena Koziol, a former postdoc at Yale University, was the victim of scientific sabotage. Now, she is suing the...
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Ancient Virus Tied to Multiple Sclerosis
29 September 2004 (All day)
An ancient virus that likely infected one of our primate ancestors 50 million years ago may contribute to the nervous system damage that causes multiple sclerosis (MS). A snippet of the virus's DNA, now embedded in the human genome, boosts production of damaging compounds in the brains of mice with a condition like MS, according to a report in the October issue of Nature Neuroscience.
MS is a debilitating neurological disease caused by the destruction of oligodendrocytes, cells that build the myelin sheaths that surround the signal transmitting axons of neurons. Damaged sheaths lead to the primary symptoms, including muscle spasms, vision impairments, and memory problems. Some scientists have suggested that infectious agents such as viruses or bacteria spark an autoimmune response that causes the disease.
The new study suggests a novel alternative: that the culprit could already be hiding in human DNA. Approximately 8% of the human genome is made up of DNA from viruses that slipped in their genetic material as our ancestors evolved. Called human endogenous retroviruses (HERVs), the vast majority of these ancient viruses are no longer functional. One exception is HERV-W. It carries instructions for making the protein syncytin, a critical element in the formation of the placenta. But HERV-W may have a dark side too.
An international team led by Christopher Power, a neurologist at the University of Calgary, found that levels of syncytin were three times higher in the brains of 16 cadavers with MS than in controls, suggesting that the protein might be a factor in the disease. In experiments with cultured human brain cells, the team then found that overproduction of syncytin can lead to the release of free radicals, charged molecules that damage oligodendrocytes. The researchers could prevent the damage in mice with MS by force-feeding them an antioxidant known as ferulic acid. Researchers still aren't sure what causes the abnormal excess of syncytin in the first place, however.
The study is "potentially groundbreaking," says Tim Coetzee, a researcher at the National Multiple Sclerosis Society who hopes the focus on antioxidants could one day lead to new treatments. And Mark Mattson, a neuroscientist at the National Institute on Aging, believes the study "opens the way" for future studies into how "foreign DNA can impact human disease."