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Items: 1 to 20 of 101


Upregulation of mouse genes in HSV-1 latent TG after butyrate treatment implicates the multiple roles of the LAT-ICP0 locus.

Clement C, Bhattacharjee PS, Kumar M, Foster TP, Thompson HW, Hill JM.

Invest Ophthalmol Vis Sci. 2011 Mar 28;52(3):1770-9. doi: 10.1167/iovs.09-5019. Print 2011 Mar.


Heat-induced reactivation of HSV-1 in latent mice: upregulation in the TG of CD83 and other immune response genes and their LAT-ICP0 locus.

Clement C, Bhattacharjee PS, Kaufman HE, Hill JM.

Invest Ophthalmol Vis Sci. 2009 Jun;50(6):2855-61. doi: 10.1167/iovs.08-2430. Epub 2009 Jan 17.


HSV-1 migration in latently infected and naive rabbits after penetrating keratoplasty.

Zheng X, Marquart ME, Loustch JM, Shah P, Sainz B, Ray A, O'Callaghan RJ, Kaufman HE, Hill JM.

Invest Ophthalmol Vis Sci. 1999 Oct;40(11):2490-7.


Microarray analysis of host gene expression for comparison between naïve and HSV-1 latent rabbit trigeminal ganglia.

Clement C, Popp MP, Bloom DC, Schultz G, Liu L, Neumann DM, Bhattacharjee PS, Hill JM.

Mol Vis. 2008 Jul 3;14:1209-21.


Microarray analysis in the HSV-1 latently infected mouse trigeminal ganglion.

Higaki S, Deai T, Fukuda M, Shimomura Y.

Cornea. 2004 Nov;23(8 Suppl):S42-7.


Changes to euchromatin on LAT and ICP4 following reactivation are more prevalent in an efficiently reactivating strain of HSV-1.

Creech CC, Neumann DM.

PLoS One. 2010 Nov 4;5(11):e15416. doi: 10.1371/journal.pone.0015416.


Increased neurovirulence and reactivation of the herpes simplex virus type 1 latency-associated transcript (LAT)-negative mutant dLAT2903 with a disrupted LAT miR-H2.

Jiang X, Brown D, Osorio N, Hsiang C, BenMohamed L, Wechsler SL.

J Neurovirol. 2016 Feb;22(1):38-49. doi: 10.1007/s13365-015-0362-y. Epub 2015 Jun 12.


Effect of immunosuppression on gene expression in the HSV-1 latently infected mouse trigeminal ganglion.

Higaki S, Gebhardt BM, Lukiw WJ, Thompson HW, Hill JM.

Invest Ophthalmol Vis Sci. 2002 Jun;43(6):1862-9.


During herpes simplex virus type 1 infection of rabbits, the ability to express the latency-associated transcript increases latent-phase transcription of lytic genes.

Giordani NV, Neumann DM, Kwiatkowski DL, Bhattacharjee PS, McAnany PK, Hill JM, Bloom DC.

J Virol. 2008 Jun;82(12):6056-60. doi: 10.1128/JVI.02661-07. Epub 2008 Apr 9.


Replication, establishment of latent infection, expression of the latency-associated transcripts and explant reactivation of herpes simplex virus type 1 gamma 34.5 mutants in a mouse eye model.

Spivack JG, Fareed MU, Valyi-Nagy T, Nash TC, O'Keefe JS, Gesser RM, McKie EA, MacLean AR, Fraser NW, Brown SM.

J Gen Virol. 1995 Feb;76 ( Pt 2):321-32.


Reactivation of HSV-1 following explant of tree shrew brain.

Li L, Li Z, Li X, Wang E, Lang F, Xia Y, Fraser NW, Gao F, Zhou J.

J Neurovirol. 2016 Jun;22(3):293-306. doi: 10.1007/s13365-015-0393-4. Epub 2015 Oct 26.


CTCF-dependent chromatin boundary element between the latency-associated transcript and ICP0 promoters in the herpes simplex virus type 1 genome.

Chen Q, Lin L, Smith S, Huang J, Berger SL, Zhou J.

J Virol. 2007 May;81(10):5192-201. Epub 2007 Jan 31.


A neuron-specific host microRNA targets herpes simplex virus-1 ICP0 expression and promotes latency.

Pan D, Flores O, Umbach JL, Pesola JM, Bentley P, Rosato PC, Leib DA, Cullen BR, Coen DM.

Cell Host Microbe. 2014 Apr 9;15(4):446-56. doi: 10.1016/j.chom.2014.03.004.

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