Influenza, COVID-19 may fuel Parkinson’s processes, finds CCMB
A CCMB study has identified how RNA viruses may trigger alpha-synuclein aggregation linked to Parkinson’s disease and how the DDX39A protein may help limit the damage.
Published - September 29, 2026 08:34 pm IST - HYDERABAD
A new study by scientists at the CSIR-CCMB has shed light on how certain RNA viruses may trigger processes linked to Parkinson’s disease. | Photo Credit: Representational Photo
Infections such as influenza and COVID-19 may increase the risk of neurodegenerative disorders, including Parkinson’s disease. However, the biological link between viral infections and brain degeneration has remained poorly understood.
A new study by scientists at the CSIR-Centre for Cellular and Molecular Biology (CCMB) has shed light on how certain RNA viruses may trigger processes linked to Parkinson’s disease. The researchers have also identified a natural cellular defence mechanism that can help limit the damage.
The team, led by Swasti Raychaudhuri, studied how infections caused by RNA viruses, including influenza and SARS-CoV-2, trigger molecular changes associated with neurodegeneration. Such diseases are often characterised by the buildup of abnormal protein deposits in the brain.
These abnormal protein clumps disrupt communication between neurons, impairing their normal function over time. Unlike humans, whose genetic material is stored as DNA, these viruses carry their genetic information in RNA.
The study focused on alpha-synuclein, a protein that can form toxic aggregates in the brains of people with Parkinson’s disease. The researchers examined whether viral infections could accelerate the formation of these protein clumps.
The viral RNA can fold into specialised three-dimensional structures called RNA G-quadruplexes (rG4s).
The researchers found that when viruses infect cells, these rG4 structures can bind to alpha-synuclein and promote its aggregation, a process associated with Parkinson’s disease.
However, the study also identified a protective response in infected cells. A protein called DDX39A, which is normally found in the cell nucleus, moves into the cytoplasm during infection and interacts with both alpha-synuclein and the viral rG4 structures.
DDX39A can unwind these viral RNA structures, reducing the virus’s ability to replicate and slowing the formation of harmful alpha-synuclein aggregates.
“The virus fails to replicate when its RNA structures are dismantled. This lowers the viral load and effectively slows alpha-synuclein amyloid formation,” said Aanchal, the study’s first author.
Mr. Raychaudhuri said the balance between harmful and protective cellular responses ultimately determines the outcome. While cells have mechanisms to fight viral infections and prevent the buildup of abnormal proteins, certain conditions may favour protein aggregation.
The researchers stressed that not every viral infection will lead to neurodegeneration. However, repeated viral infections could increase the likelihood of harmful changes accumulating over time. The team is now investigating how seemingly routine viral infections could contribute to the development of Parkinson’s disease years later, informed a press release.
Published - September 29, 2026 08:34 pm IST
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