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Hhv infected cell polypeptide 0

The meaning of «hhv infected cell polypeptide 0»

Human Herpes Virus (HHV) Infected Cell Polypeptide 0 (ICP0) is a protein, encoded by the DNA of herpes viruses. It is produced by herpes viruses during the earliest stage of infection, when the virus has recently entered the host cell; this stage is known as the immediate-early or α ("alpha") phase of viral gene expression.[1] During these early stages of infection, ICP0 protein is synthesized and transported to the nucleus of the infected host cell. Here, ICP0 promotes transcription from viral genes, disrupts structures in the nucleus known as nuclear dots or promyelocytic leukemia (PML) nuclear bodies,[2] and alters the expression of host and viral genes in combination with a neuron specific protein.[3][4] At later stages of cellular infection, ICP0 relocates to the cell cytoplasm to be incorporated into new virion particles.[5]

ICP0 was identified as an immediate-early polypeptide product of Herpes simplex virus-1 (HSV-1) infection in 1976.[6] The gene, in HSV-1, from which ICP0 is produced is known as HSV-1 α0 ("alpha zero"), Immediate Early (IE) gene 1, or simply as the HSV-1 ICP0 gene. The HSV-1 ICP0 gene was characterized and sequenced in 1986.[7] This sequence predicted a 775 amino acid sequence with a molecular weight of 78.5 KDa.[7][8] At the time of gene isolation, ICP0 was known as IE110 as gel electrophoresis experiments performed prior to obtaining the gene sequence indicated the ICP0 protein weighed 110 kDa. Post-translational modifications, such as phosphorylation or sumoylation, were presumed to account for the actual protein size appearing 30 kDa larger than that of the predicted amino acid sequence.

ICP0 co-localizes with α-tubulin, and dismantles host cell microtubule networks once it translocates to the cytoplasm.[9]

In HSV-1 infected cells, ICP0 activates transcription of many viral and cellular genes. It acts synergistically with HSV-1 immediate early (IE) protein, ICP4, and is essential for reactivation of latent herpes virus and viral replication.[10]

ICP0 is responsible for overcoming a variety of cellular antiviral responses. After translocating to the nucleus early in infection, ICP0 promotes degradation of many cellular antiviral genes, including those for nuclear body-associated proteins promyelocytic leukemia protein (PML) and Sp100, causing disruption of PML nuclear bodies and reduced cellular antiviral capacity.[11][12] ICP0 also inhibits the activity of IFN regulatory factors (IRF3) and IRF7, which are key transcription factors that induce production of antiviral cytokines called interferons.[13] Barriers to viral replication induced by interferons can also be overcome by the action of ICP0.[14] This function of ICP0 also prevents production of RNase L, an enzyme that degrades single-stranded viral and cellular RNAs and induces host cell apoptosis in virus infected cells.[15]

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