Disease relevance of US10

• DNA sequence analyses of the IR5 gene region revealed an ORF of 236 amino acids (24,793 Da) that showed significant homology to ORF64 of varicella-zoster virus and ORF3 of EHV-4 both of which map within the inverted repeats and to the US10 ORF of herpes simplex virus type 1 (HSV-1) which maps within the unique short segment [1].
• These ORFs are conserved in a similar arrangement with those of HSV-1, except for US10 which is transposed in the Us regions of all three MDV serotypes [2].
• Consequently, no capsids were found in the cytoplasm, resulting in an inhibition of virion morphogenesis [3].
• The myristylated virion proteins of herpes simplex virus type 1: investigation of their role in the virus life cycle [4].
• The virion half-life of hepatitis B virus (HBV) is currently estimated at approximately 1 day [5].

High impact information on US10

• A virion protein of herpes simplex virus type 1 (HSV-1) specifically and potently activates transcription of the viral immediate early genes [6].
• Herpes simplex virus VP16 rescues viral mRNA from destruction by the virion host shutoff function [7].
• The fragmentation and dispersal of the Golgi apparatus was a late event in the reproductive cycle coinciding with virion assembly, processing of viral glycoproteins, and exocytosis from infected cells [8].
• This new value is consistent with virion half-life estimates for HIV and hepatitis C virus [5].
• We demonstrate that the acidic activation domain of virion protein 16 interferes both with basal transcription from TATA-box promoters and promoters activated by various trans-activators in two different mammalian cell-free transcription systems [9].

Chemical compound and disease context of US10

• By fusing the tet repressor with the activating domain of virion protein 16 of herpes simplex virus, a tetracycline-controlled transactivator (tTA) was generated that is constitutively expressed in HeLa cells [10].
• Pseudorabies virus glycoprotein L is necessary for virus infectivity but dispensable for virion localization of glycoprotein H [11].
• ISIS 1082, a phosphorothioate oligonucleotide targeted to a translation initiation codon of herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) virion capsid protein UL13 inhibits in vitro viral replication [12].

Biological context of US10

• The herpes simplex virus 1 RNA binding protein US11 is a virion component and associates with ribosomal 60S subunits [13].
• At least one virion-associated protein is involved in inhibition of STAT1 tyrosine phosphorylation [14].
• Transactivation by a complex of the cellular transcription factor Oct-1 and the virion protein Vmw65 is necessary for the high-level activity of the HSV immediate-early promoters during lytic infection [15].
• The virion host shutoff protein of herpes simplex virus inhibits reporter gene expression in the absence of other viral gene products [16].
• VZV gK, an essential glycoprotein that is conserved among the alphaherpesviruses, is believed to participate in membrane fusion and cytoplasmic virion morphogenesis based on analogy to its HSV-1 homolog [17].

Anatomical context of US10

• US11 protein associates with ribosomes both late in infection at the time of its synthesis and at the time of infection after its introduction into the cytoplasm by the virion [13].
• With a virion DNA probe, three transcripts (2.0, 1.5, and 1.45 kilobases [kb]) were detected by Northern blot (RNA blot) analysis of RNAs isolated from the ganglia of latently infected mice [18].
• Herpes simplex virus type 1 (HSV-1) glycoprotein B (gB) is a major component of infected cell membranes and virion envelopes [19].
• These recombinant baculoviruses expressed a protein that was slightly smaller than virion HSV-1 gD made in Vero cells [20].

Associations of US10 with chemical compounds

• This US11 protein, which has phosphates on multiple serine residues, is brought into the cell by the virion and found to be present within ribosome fractions early after infection [21].
• Treatment with phosphonoacetate which inhibits viral DNA synthesis and hence virion morphogenesis induced a striking increase in the time course of conversion of immature gC, gD, and gB to fully glycosylated forms when measured late in the infection [22].
• The effects of gallic acid (3,4,5-trihydroxybenzoic acid) and its alkyl esters on virus growth and virion infectivity were examined [23].
• A pH-sensitive activity, likely to be a virion fusion glycoprotein, is also required [24].

Analytical, diagnostic and therapeutic context of US10

• This communication outlines a novel approach to viral inactivation by specific solvent delipidation which modifies the whole virion rendering it non-infective, but antigenic [25].

References