Disease relevance of US10

• METHODS: From 30 patients with RHK, sequential corneal HSV-1 isolates were genotyped by PCR amplification of the hypervariable regions located within the HSV-1 genes US1, US10/11, and US12 [1].
• The virion host shutoff protein (UL41) of herpes simplex virus 1 is an endoribonuclease with a substrate specificity similar to that of RNase A [2].
• Using a transfection/infection-based virion incorporation assay, residues 165-270 of VP22 fused to GFP competed efficiently with wild-type VP22 for packaging into assembling virus particles [3].
• L-particles are noninfectious virion-related particles that lack the nucleocapsid but do contain tegument and envelope [4].
• No virion-associated inhibition of cellular protein synthesis or vhs-induced cellular mRNA degradation was detected in cells infected with any of three EHV-1 strains (Ab4, KyA, and KyD) at multiplicities of infection at which HSV-1 strain F exhibited maximal vhs activity [5].

High impact information on US10

• Differential regulation of octamer-containing cellular genes by the herpes simplex virus virion protein Vmw65 is mediated by sequence differences in the octamer element [6].
• We conclude that (i) three virion proteins are capable of binding RNA; (ii) the packaged RNA can be expressed in newly infected cells; and (iii) the U(L)47 protein was earlier reported to shuttle from nucleus to the cytoplasm and may transport RNA [7].
• The virion half-life of hepatitis B virus (HBV) is currently estimated at approximately 1 day [8].
• This new value is consistent with virion half-life estimates for HIV and hepatitis C virus [8].
• These results show for the first time that sialic acids on HSV-1 virions play an important role in infection and suggest that targeting virion sialic acids may be a valid antiviral drug development strategy [9].

Chemical compound and disease context of US10

• This finding is in marked contrast to a similar mutant of the related alphaherpesvirus, pseudorabies virus (A. R. Brack, J. M. Dijkstra, H. Granzow, B. G. Klupp, and T. C. Mettenleiter, J. Virol. 73:5364-5372, 1999), and suggests that the glycoprotein requirements for virion assembly may vary among different members of this family of viruses [10].
• alpha trans-inducing factor (alpha TIF, VP16, Vmw65) is an essential structural protein of herpes simplex virus, being required for virion assembly [11].
• The effect of triterpenoid compounds on uninfected and herpes simplex virus-infected cells in culture. III. Ultrastructural study of virion maturation [12].

Biological context of US10

• A feature of the cascade regulation of herpes simplex virus 1 gene expression in productive infection is that the first genes to be expressed, the alpha genes, are transactivated by a structural component of the virion designated as the alpha transinducing factor (alpha TIF) [13].
• We propose a model for infectious entry of HSV-1 by a series of interactions between the virion envelope and the cell plasma membrane that trigger virion disassembly, membrane fusion, and capsid penetration [14].
• In all virus-cell systems analyzed, similar observations were made concerning the different stages of virion morphogenesis [15].
• Cloned BamHIf had the same specificity as the virion component, since it stimulated thymidine kinase expression only from chimaeric plasmids which contained functional IE-specific regulatory sequences [16].
• The equine herpesvirus 1 (EHV-1) homolog of the herpes simplex virus type 1 (HSV-1) tegument phosphoprotein, alphaTIF (Vmw65; VP16), was identified previously as the product of open reading frame 12 (ORF12), was shown to trans-activate immediate-early (IE) gene promoters, and was described as a 60-kDa virion component designated ETIF [17].

Anatomical context of US10

• The site of the defect in retrograde spread remains to be determined; however, infection of rat superior cervical ganglia neurons in vitro indicates that gE is required to target virion components to the axon initial segment [18].
• Input virion-associated VP13/14 and VP16 localized to the nucleus early in infection, while VP1/2 localized to the nuclear envelope of the cell and VP22 could not be detected using monoclonal antibody P43 [19].
• The cell line expressing VZV ORF61 enhanced the infectivity of HSV-1 virion DNA [20].
• Unlike KOS infected Vero cells, virion-containing vacuoles were observed in the cytoplasm at 12 h p.i. and extracellular virions were concentrated at cell-cell junctions of 424 or 490 infected cells but not in the perinuclear region [21].

Associations of US10 with chemical compounds

• The phosphorylation of virion-associated VP13/14, VP16, and VP22 was demonstrated in cells infected in the presence of cycloheximide [22].
• At least one virion-associated protein is involved in inhibition of STAT1 tyrosine phosphorylation [23].
• The effects of gallic acid (3,4,5-trihydroxybenzoic acid) and its alkyl esters on virus growth and virion infectivity were examined [24].

Other interactions of US10

• Cells infected with the UL13-negative mutants were shown to contain much lower levels than normal of the UL41 gene product, which is known to be required for virion host shutoff [25].
• Analysis of isolated mature HSV virions and light particles revealed that the UL37 protein is a component of the virion [26].

Analytical, diagnostic and therapeutic context of US10

• Western blotting suggested that virion-associated VP13/14, VP16 and VP22 were stable in infected cells whereas VP1/2 appeared to be processed or modified [19].
• By using UV cross-linking, equilibrium density centrifugation, and immunoprecipitation, we obtained evidence consistent with the interpretation that delta antigen and genomic RNA form a stable ribonucleoprotein (RNP) complex within the virion [27].
• This communication outlines a novel approach to viral inactivation by specific solvent delipidation which modifies the whole virion rendering it non-infective, but antigenic [28].
• Purification of herpes simplex virus type 1 by density gradient centrifugation and estimation of the sedimentation coefficient of the virion [29].

References