Herpesvirus infection alters the structure and function of mitochondria in the host cell
最近審查：14.06.2024
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Researchers from the University of Jyväskylä have discovered that infection with a herpes virus alters the structure and normal function of mitochondria in the host cell. These new data will help to understand the interaction between the herpesvirus and host cells. The knowledge gained can be used in developing treatments for viral diseases.
Herpesviruses not only cause serious disease, but are also promising candidates for oncolytic therapy. HSV-1 infection depends on nuclear DNA replication, transcription machinery, and host cell mitochondrial metabolism. At the Department of Biological and Environmental Sciences at the University of Jyväskylä, Associate Professor Maja Vihinen-Ranta and her research group studied the temporal changes in mitochondria as HSV-1 infection progresses from early to late stages.
New data on the interaction of herpesvirus and host cell
Recent studies indicate that infection results in significant transcriptional modification of genes encoding proteins involved in the mitochondrial network, such as the respiratory chain, apoptosis, and mitochondrial structural organization. The results indicate significant changes in mitochondrial structure and function, including changes in mitochondrial morphology and distribution, thickening and shortening of cristae, increased number and area of contact sites between mitochondria and the endoplasmic reticulum, and increased mitochondrial calcium ion content and proton leakage. “Our results show how the progression of infection shifts the balance from healthy to diseased cells and leads to profound disruptions in mitochondrial homeostasis.” This could provide additional insights into the interaction between the herpesvirus and host cells, says Associate Professor Maja Vihinen-Ranta from the University of Jyväskylä. She continues to say that this knowledge can be used to develop treatments for viral diseases.
The results of the study were published on the page of PLOS magazine