Herpesvirus Infection Reshapes Mitochondrial Architecture and Disrupts Metabolic Processes

Researchers from the University of Jyväskylä have found that herpesvirus infection alters the normal structure and function of host cell mitochondria. This new data contributes to our understanding of how the herpesvirus interacts with host cells, and this knowledge can be used to develop antiviral treatments.

In addition to being major disease causes, herpesviruses show promise as candidates for oncolytic therapy. The host cell's transcription machinery, nuclear DNA replication, and mitochondrial metabolism are all necessary for HSV-1 infection. Maija Vihinen-Ranta, a docent in the Department of Biological and Environmental Science at the University of Jyväskylä, studied the time-dependent alterations in mitochondrial structure during the progression of HSV-1 infection from early to late stages.

New Information on the Interaction Between the Herpesvirus and the Host Cell

According to recent studies, the infection considerably alters the transcription of genes that code for proteins involved in the mitochondrial network, including the respiratory chain, apoptosis, and the structural makeup of mitochondria.

The results show that the infection causes major changes in the morphology and distribution of mitochondria, the thickening and shortening of cristae, an increase in the number and area of contact sites between the mitochondria and the endoplasmic reticulum, and an increase in the calcium ion content and proton leakage of mitochondria.

The findings demonstrate how the spread of infection causes significant disruptions to mitochondrial homeostasis and a shift in the balance from healthy to sick cells. This may provide more insight into how the herpes virus interacts with host cells, according to the University of Jyväskylä docent Maija Vihinen-Ranta. She goes on to say that the creation of viral treatments can make use of this knowledge.

Journal reference:

Leclerc, S., et al. (2024) Progression of herpesvirus infection remodels mitochondrial organization and metabolism. PLoS Pathogens. doi.org/10.1371/journal.ppat.1011829


The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of AZoLifeSciences.
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