about
The role of the CoREST/REST repressor complex in herpes simplex virus 1 productive infection and in latencyThe stability of herpes simplex virus 1 ICP0 early after infection is defined by the RING finger and the UL13 protein kinase.Characterization of a recombinant herpes simplex virus 1 designed to enter cells via the IL13Ralpha2 receptor of malignant glioma cells.Disruption of HDAC/CoREST/REST repressor by dnREST reduces genome silencing and increases virulence of herpes simplex virusCation-independent mannose 6-phosphate receptor blocks apoptosis induced by herpes simplex virus 1 mutants lacking glycoprotein D and is likely the target of antiapoptotic activity of the glycoprotein.Truncated forms of glycoprotein D of herpes simplex virus 1 capable of blocking apoptosis and of low-efficiency entry into cells form a heterodimer dependent on the presence of a cysteine located in the shared transmembrane domains.Engineered herpes simplex virus 1 is dependent on IL13Ralpha 2 receptor for cell entry and independent of glycoprotein D receptor interaction.The CoREST/REST repressor is both necessary and inimical for expression of herpes simplex virus genes.Construction and properties of a herpes simplex virus 1 designed to enter cells solely via the IL-13alpha2 receptorThe domains of glycoprotein D required to block apoptosis induced by herpes simplex virus 1 are largely distinct from those involved in cell-cell fusion and binding to nectin1Patterns of accumulation of miRNAs encoded by herpes simplex virus during productive infection, latency, and on reactivation.HSV-1 gene expression from reactivated ganglia is disordered and concurrent with suppression of latency-associated transcript and miRNAsSeparation of receptor-binding and profusogenic domains of glycoprotein D of herpes simplex virus 1 into distinct interacting proteins.Induction of apoptosis accelerates reactivation of latent HSV-1 in ganglionic organ cultures and replication in cell cultures.HSV carrying WT REST establishes latency but reactivates only if the synthesis of REST is suppressed.miR-H28 and miR-H29 expressed late in productive infection are exported and restrict HSV-1 replication and spread in recipient cellsModulation of reactivation of latent herpes simplex virus 1 in ganglionic organ cultures by p300/CBP and STAT3.Checkpoints in productive and latent infections with herpes simplex virus 1: conceptualization of the issues.The 3 facets of regulation of herpes simplex virus gene expression: A critical inquiry.
P50
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P50
name
Guoying Zhou
@en
type
label
Guoying Zhou
@en
prefLabel
Guoying Zhou
@en