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Gene Review

UL53  -  type 3 membrane protein; contains a signal...

Human herpesvirus 1

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Disease relevance of UL53

  • Mutations in the UL53 gene of HSV-1 abolish virus neurovirulence to mice by the intracerebral route of infection [1].
  • Syncytial mutations in the herpes simplex virus type 1 gK (UL53) gene occur in two distinct domains [2].
  • The pseudorabies virus (PrV) gene homologous to herpes simplex virus type 1 (HSV-1) UL53, which encodes HSV-1 glycoprotein K (gK), has recently been sequenced (J. Baumeister, B. G. Klupp, and T. C. Mettenleiter, J. Virol. 69:5560-5567, 1995) [3].
  • The second ORF of 336 aa, located at map units 0.075 to 0.08, has a predicted molecular weight (MW) of 38 kDa with significant homology to glycoprotein K (gK) of HSV-1 (UL53), ORF5 of VZV and ORF6 of EHV-1 [4].

High impact information on UL53

  • Analysis of the transcription pattern of HSV-1 UL52 and UL53 genes [5].
  • Therefore, it was suggested that the translation of the UL53 open reading frame (ORF) starts at an internal initiation codon that is located 55 codons downstream of the putative one [5].
  • The cell fusion protein, the product of the UL53 gene, is responsible for intracerebral (IC) pathogenicity of HSV-1 [1].
  • The nucleotide sequence of the UL53 gene of HSV-1 strains R15 (apathogenic) and R19 (pathogenic) was determined and compared to that of other pathogenic strains [1].
  • Syn strains HSZP and ANGpath [correction of ANG] of herpes simplex virus type 1 do not contain mutations in the regions of UL53 gene relevant to syncytium formation [6].

Biological context of UL53

  • Recombinant HSV-1 R15 is apathogenic to mice by the IC route of inoculation, while intratypic recombinants, in which the UL53 gene in R15 was replaced by an analogous sequence from the pathogenic strain R19, regained IC pathogenicity [1].
  • Parallel sequencing of UL53 gene of four strains of herpes simplex virus type 1 (HSV-1), two of which (HSZP and ANGpath) were of the syn phenotype while another two (KOS and 17) were of the non-syn phenotype, showed in three strains amino acid mutations unrelated to the already described syn1 glycoprotein K (gK) mutations (Dolter et al., 1994) [6].

Other interactions of UL53

  • An RNase protection experiment was designed to determine the 5' termini of both the UL52 and UL53 mRNAs [5].

Analytical, diagnostic and therapeutic context of UL53

  • Northern blot hybridization of RNA extracted from BSC-1 cells infected with several HSV-1 strains indicated that all of the virus strains tested expressed equal amounts of UL53 mRNA in infected cell cultures [1].


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