News Release

Progression of herpesvirus infection remodels mitochondrial organization and metabolism

Peer-Reviewed Publication

University of Jyväskylä - Jyväskylän yliopisto

The progression of infection leads to thinner and rougher mitochondria


Cryo-soft X-ray tomography 3D reconstructions of segmented mitochondria (brown) in the cytoplasm around the nucleus (blue) in herpes simplex virus type 1 infected cell. 

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Credit: Maija Vihinen-Ranta

Researchers at the University of Jyväskylä have found that herpesvirus infection modifies the structure and normal function of the mitochondria in the host cell. The new information will help to understand the interaction between herpesvirus and host cells. Knowledge can be utilized in the development of viral treatments. 

Herpesviruses not only cause significant diseases but are also promising candidates for oncolytic therapy. The HSV-1 infection depends on the nuclear DNA replication, transcription machinery, and mitochondrial metabolism of the host cell. In the Department of Biological and Environmental Science of the University of Jyväskylä, docent Maija Vihinen-Ranta, with her research team, investigated time-dependent mitochondrial changes as HSV-1 infection proceeds from early to late infection.

New information on the interaction between the herpesvirus and the host cell

Recent research shows that the infection leads to significant transcriptional modification of genes encoding proteins involved in the mitochondrial network, such as the respiratory chain, apoptosis, and the structural organization of mitochondria. Findings indicate that the infection leads to significant alterations in mitochondrial structure and function, including changes in mitochondrial morphology and distribution, thickening and shortening of cristae, an increase in the number and area of contact sites between mitochondria and the endoplasmic reticulum, as well as a rise in mitochondrial calcium ion content and proton leak.

- Our results show how the progression of infection shifts the balance from healthy to diseased cells and leads to profound perturbations in mitochondrial homeostasis. This can yield further knowledge about the interaction between herpesvirus and host cells, states docent Maija Vihinen-Ranta from the University of Jyväskylä. She continues to say that this knowledge can be utilized in the development of viral treatments.

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