Publications by authors named "Esteban Flores Cortes"
Unlabelled: Herpes simplex virus 1 (HSV-1) transcription is restricted in latently infected neurons and the genomes are in mostly silenced chromatin, whereas all viral genes are transcribed in lytically infected cells, in which the genomes are dynamically chromatinized. Epigenetic regulation modulates HSV-1 transcription during lytic, latent, and reactivating infections but the precise mechanisms are not fully defined. Nucleosomes are dynamic: they slide, breathe, assemble, and disassemble.
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- HSV-1 is a virus that can hide in our bodies and come back later, making it hard to treat with medicine because it doesn’t act like a regular virus all the time.
- Scientists believe how the virus hides and returns has a lot to do with something called epigenetics, which involves changes in how genes are used.
- Some recent studies suggest that the viruses and our cells work differently when it comes to epigenetics, which might help researchers find new ways to make medicine that can stop the virus.
During latent infections with herpes simplex virus 1 (HSV-1), viral transcription is restricted and the genomes are mostly maintained in silenced chromatin, whereas in lytically infected cells all viral genes are transcribed and the genomes are dynamically chromatinized. Histones in the viral chromatin bear markers of silenced chromatin at early times in lytic infection or of active transcription at later times. The virion protein VP16 activates transcription of the immediate-early (IE) genes by recruiting transcription activators and chromatin remodelers to their promoters.
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