Herpes rewires energy metabolism in human neurons, imaging study reveals
Herpes simplex virus type 1 (HSV-1), the virus best known for causing cold sores, infects a large portion of the world's population and can remain dormant in nerve cells for decades. In recent years, researchers have found evidence linking HSV-1 to neurological conditions such as Alzheimer's disease, but scientists still do not fully understand how the virus affects the brain.
This study, published in Neurophotonics, reveals how the herpes simplex virus type 1 (HSV-1), responsible for cold sores, alters the energy metabolism of human neurons. Using a 3D model of human brain tissue, researchers observed that HSV-1 initially boosts energy production in infected neurons. However, over time, this heightened activity is accompanied by signs of stress and impaired mitochondrial function.
The research, led by Maria Savvidou, a senior researcher at Tufts University, indicates that HSV-1 changes neuronal metabolism in a way that could potentially contribute to neurological diseases. The virus causes infected neurons to initially increase glycolytic and mitochondrial energy metabolism, with increased lactate release and later lactate utilization as an alternative fuel source.
Despite this metabolic reprogramming, infected neurons remained viable throughout the 10-day experiment. The study also found that HSV-1 infection led to oxidative stress, lipofuscin accumulation, and altered mitochondrial function, even though cell viability was preserved. These findings suggest that HSV-1 may induce a gradual but substantial shift in neuronal metabolism that could serve as an early warning sign of neurological disease.
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