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• W2080846870 endingPage "16059" @default.
• W2080846870 startingPage "16055" @default.
• W2080846870 abstract "Herpes simplex virus (HSV) persists in its human host and evades the immune response by undergoing a latent infection in sensory neurons, from which it can reactivate periodically. HSV expresses >80 gene products during productive (“lytic”) infection, but only the latency-associated transcript ( LAT ) gene is expressed at abundant levels during latent infection. The LAT gene has been shown to repress lytic-gene expression in sensory neurons. In this study, we use chromatin immunoprecipitation to show that HSV lytic-gene promoters become complexed with modified histones associated with heterochromatin during the course of establishment of latent infection. Experiments comparing LAT-negative and LAT-positive viruses show that a function encoded by the LAT gene increases the amount of dimethyl lysine 9 form of histone H3 or heterochromatin and reduces the amount of dimethyl lysine 4 form of histone H3, a part of active chromatin, on viral lytic-gene promoters. Thus, HSV, and in particular the HSV LAT gene, may manipulate the cellular histone modification machinery to repress its lytic-gene expression and contribute to the persistence of its genome in a quiescent form in sensory neurons." @default.
• W2080846870 created "2016-06-24" @default.
• W2080846870 creator A5034709604 @default.
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• W2080846870 date "2005-10-24" @default.
• W2080846870 modified "2023-10-06" @default.
• W2080846870 title "Herpesviral latency-associated transcript gene promotes assembly of heterochromatin on viral lytic-gene promoters in latent infection" @default.
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• W2080846870 doi "https://doi.org/10.1073/pnas.0505850102" @default.
• W2080846870 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1266038" @default.
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