Herpes Virus Protein ICP4 Liquefies Host Nuclei to Speed Replication, Study Finds
Blocking the fluidizing activity cut new virus production about four-fold in engineered cell experiments.
Overview
- Published March 5 in Molecular Cell, the NYU Langone–led study used glowing nucGEM nanoparticles and live microscopy to quantify increased nuclear fluidity after HSV-1 infection.
- Introducing ICP4 alone increased chromatin motion without a corresponding rise in transcription, indicating a physical remodeling role rather than gene activation.
- The more fluid nuclear environment enabled small viral condensates to merge into larger replication factories that concentrate the virus’s production machinery.
- Interfering with ICP4’s ability to fluidize the nuclear compartment reduced the rate of new virion production by roughly four-fold in the study’s models.
- Researchers are now probing the precise mechanism of ICP4-driven fluidization and testing whether other nuclear-replicating viruses use the same strategy.