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← All articlesEditorial brief · abstract-levelScore 89/100Confidence high
biorxiv2026-09-03infectionfusionmtDNAimport

HSV-1 shreds mtDNA and OPA1 so mitochondria shrink to the nucleus and serve the virus

HSV-1 uses UL12.5 to erase mitochondrial DNA and the biogenesis factors PGC-1alpha and TFAM. Independently it activates OMA1 to cleave OPA1, drops MFN2, and down-modulates TIM23, so the network fragments and huddles perinuclearly. Fail to make those changes and the infection suffers. Mitophagy is still held off (abstract cuts there).

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Signal profile (abstract-level)

infection · fusion · mtDNA · import

Score 89/100BIORXIVhigh confidenceinfection
89
Importance
70
Mito signal
95
Dysfunction
75
Evidence
15
Translational

Editorial signal profile from the abstract (importance score, mito keywords, dysfunction tags, evidence density, translational cues). Not a figure reproduced from the preprint PDF.

Finding. Herpes simplex virus 1 does not politely share a cell's mitochondria. Saud, Kalamvoki and colleagues split the attack. UL12.5 takes out mitochondrial DNA and the biogenesis pair PGC-1alpha and TFAM. Separate, UL12.5-independent tricks turn OMA1 on so OPA1 is cleaved, drop MFN2, and turn TIM23 down. Fusion dies. The network shrinks and parks by the nucleus, a plausible energy and envelopment depot. If the virus cannot force those changes, infection suffers. Mitophagy is somehow blocked; the abstract ends mid-sentence.

Score 89. Named viral module, named host GTPases and import, a fitness cost. High confidence for the split as stated.

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Source preprint

Herpes simplex virus 1 subverts the mitochondrial network to support the infection: A lesson on mitochondrial versatility

10.64898/2026.09.02.748825

Saud R, Foster-Lemieur K, Duguay B, Swerdlow R, Kalamvoki M.

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