ArticleCells2026
New Insights into Parthanatos as Programmed Cell Death During Murine Cytomegalovirus or Herpes Simplex Virus Type 1 Productive Replication in Diverse Cell Types.
Article in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Programmed cell death (PCD) pathways of innate immunity serve to protect host cells from invading viruses. Parthanatos is a novel form of PCD triggered by excessive host cell DNA damage that leads to overactivation of poly(ADP-ribose) polymerase-1 (PARP-1) which in turn stimulates poly(ADP-ribose) (PAR) polymer formation. PAR translocates to the cytoplasm, where it induces release of apoptosis-inducing factor (AIF) from mitochondria, that then travels back to the nucleus, where it mediates large-scale DNA fragmentation and cell death. Little information is available regarding parthanatos as a cell death mechanism to dampen herpesvirus replication at the host cell level. A series of studies were therefore performed to clarify a possible role for parthanatos during productive replication of murine cytomegalovirus (MCMV) and herpes simplex virus type 1 (HSV-1) in diverse cell types. These included mouse embryo fibroblasts, mouse lung fibroblasts, mouse microglial (BV-2) cells, and human retinal pigment epithelial (ARPE-19) cells. We report that PAR protein production is surprisingly cell type specific. Moreover, MCMV or HSV-1 infection may suppress parthanatos as observed for other PCD pathways, such as apoptosis, necroptosis, and pyroptosis, in a dose-dependent and cell type-specific manner. We conclude that the operation of parthanatos at the host cell level during herpesvirus replication is more complex than originally thought but offers new targets for possible therapeutic interventions.
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