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Gene Review

RL1  -  virion protein; inhibits stress-induced...

Human herpesvirus 1

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Disease relevance of RL1


High impact information on RL1

  • However, internalization is blocked completely when viruses lack the neurovirulence factor, infected cell protein 34.5, or when endocytosis is inhibited with bafilomycin A(1) or chloroquine [5].
  • The HSV gene RL1 (gamma(1)34.5; neurovirulence factor) is not present in HVP-2, as is the case for SA8 and B virus [6].
  • Herpes simplex virus type-1 (HSV1) in which the neurovirulence factor ICP34.5 is inactivated has been shown to direct tumour-specific cell lysis in several tumour models [7].
  • It has previously been demonstrated that variants of HSV-1 which are deleted in the RL1 gene and fail to produce the virulence factor ICP34.5 are potential candidates for tumour therapy [8].
  • ORF-P, the first and largest open reading frame (ORF) encoded by the L/STs, overlaps >90% of the ORF encoding ORF-34.5, a putative neurovirulence factor, which is transcribed from the opposite DNA strand [9].

Biological context of RL1

  • Although an open reading frame (ORF) was predicted in HSV-1(F) and shown to encode a polypeptide called ICP34.5, only recently has a corresponding ORF, designated RL1, been recognized in HSV-1(17) [10].
  • The second was mouse embryo testicular carcinoma F9 cells which, in the undifferentiated state, provide a reversal of phenotype; wild-type virus fails to grow but RL1-negative virus replicates efficiently [11].
  • To determine whether the HSV-1(17) ORF is expressed, we raised antipeptide sera against predicted amino acid sequences from RL1; one serum specifically recognized a 37K protein in HSV-1(17)-infected cell extracts [10].
  • 5. Hence RL1-negative mutants have the distinct advantage of providing a double hit phenomenon whereby cell death could occur by either pathway [12].
  • L/ST-4BS was completely attenuated for neurovirulence (LD50 > 10(6) PFU) relative to wild-type virus (LD50 < 900 PFU), although the four single-base-pair substitutions lie outside the coding region for the neurovirulence factor, ICP34 [9].

Anatomical context of RL1

  • Null mutants in RL1 fail to replicate in the central nervous system of mice and are therefore totally non-neurovirulent [11].
  • The first was mouse embryo fibroblast 3T6 cells, in which RL1-negative mutants are impaired and the in vivo phenotype is mimicked [11].
  • To this end, the lateral ventricle of nude mice was injected with high (2.5 x 10(7) PFU), medium (10(5) PFU), or low dose (10(3) PFU) HSV-1 variant-1716, which has a deletion in the RL-1 gene [13].

Analytical, diagnostic and therapeutic context of RL1


  1. Status of the ICP34.5 gene in herpes simplex virus type 1 strain 17. Dolan, A., McKie, E., MacLean, A.R., McGeoch, D.J. J. Gen. Virol. (1992) [Pubmed]
  2. Characterization of the herpes simplex virus type 1 strain 17+ neurovirulence gene RL1 and its expression in a bacterial system. McKie, E.A., Hope, R.G., Brown, S.M., MacLean, A.R. J. Gen. Virol. (1994) [Pubmed]
  3. Functional analysis of the herpes simplex virus type 2 strain HG52 RL1 gene: the intron plays no role in virulence. Ravi, V., Kennedy, P.G., MacLean, A.R. J. Gen. Virol. (1998) [Pubmed]
  4. Complete genome sequence of cercopithecine herpesvirus 2 (SA8) and comparison with other simplexviruses. Tyler, S.D., Peters, G.A., Severini, A. Virology (2005) [Pubmed]
  5. Selective internalization of sodium channels in rat dorsal root ganglion neurons infected with herpes simplex virus-1. Storey, N., Latchman, D., Bevan, S. J. Cell Biol. (2002) [Pubmed]
  6. The complete genome sequence of herpesvirus papio 2 (Cercopithecine herpesvirus 16) shows evidence of recombination events among various progenitor herpesviruses. Tyler, S.D., Severini, A. J. Virol. (2006) [Pubmed]
  7. ICP34.5 deleted herpes simplex virus with enhanced oncolytic, immune stimulating, and anti-tumour properties. Liu, B.L., Robinson, M., Han, Z.Q., Branston, R.H., English, C., Reay, P., McGrath, Y., Thomas, S.K., Thornton, M., Bullock, P., Love, C.A., Coffin, R.S. Gene Ther. (2003) [Pubmed]
  8. Selective astrocytic transgene expression in vitro and in vivo from the GFAP promoter in a HSV RL1 null mutant vector--potential glioblastoma targeting. McKie, E.A., Graham, D.I., Brown, S.M. Gene Ther. (1998) [Pubmed]
  9. A virus with a mutation in the ICP4-binding site in the L/ST promoter of herpes simplex virus type 1, but not a virus with a mutation in open reading frame P, exhibits cell-type-specific expression of gamma(1)34.5 transcripts and latency-associated transcripts. Lee, L.Y., Schaffer, P.A. J. Virol. (1998) [Pubmed]
  10. The herpes simplex virus type 1 strain 17 open reading frame RL1 encodes a polypeptide of apparent M(r) 37K equivalent to ICP34.5 of herpes simplex virus type 1 strain F. McKay, E.M., McVey, B., Marsden, H.S., Brown, S.M., MacLean, A.R. J. Gen. Virol. (1993) [Pubmed]
  11. Cell type and cell state determine differential in vitro growth of non-neurovirulent ICP34.5-negative herpes simplex virus types 1 and 2. Brown, S.M., Harland, J., MacLean, A.R., Podlech, J., Clements, J.B. J. Gen. Virol. (1994) [Pubmed]
  12. Selective in vitro replication of herpes simplex virus type 1 (HSV-1) ICP34.5 null mutants in primary human CNS tumours--evaluation of a potentially effective clinical therapy. McKie, E.A., MacLean, A.R., Lewis, A.D., Cruickshank, G., Rampling, R., Barnett, S.C., Kennedy, P.G., Brown, S.M. Br. J. Cancer (1996) [Pubmed]
  13. Toxicity and neuronal infection of a HSV-1 ICP34.5 mutant in nude mice. Lasner, T.M., Tal-Singer, R., Kesari, S., Lee, V.M., Trojanowski, J.Q., Fraser, N.W. J. Neurovirol. (1998) [Pubmed]
  14. Replication of the herpes simplex virus type 1 RL1 mutant 1716 in primary neuronal cell cultures--possible relevance to use as a viral vector. Kennedy, P.G., Gairns, J., MacLean, A.R. J. Neurol. Sci. (2000) [Pubmed]
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