1887

Abstract

The precise endpoints of the deletions/insertions in three variants (1704, 1705 and 1706) of herpes simplex virus type 1 (HSV-1) strain 17 have been determined by dideoxynucleotide sequence analysis. The analysis was undertaken to discover whether the three variants had arisen from the same initial event and the extent of the deletions with respect to the latency-associated transcripts (LATs) and the proposed LAT promoter region. It is not possible from the deletion boundaries to determine unequivocally whether the three variants had arisen from the same recombination event although 1706 could be descended from 1705 by illegitimate recombination. The results demonstrate that spontaneous deletions can occur at random within R, the extent of the deletions in U is constrained by the essential nature of U genes but is otherwise arbitrary and deletions in 1704 completely remove both copies of the LAT promoter region and in IR extend into the 5′ end of the LAT sequence.

Loading

Article metrics loading...

/content/journal/jgv/10.1099/0022-1317-72-9-2311
1991-09-01
2024-04-25
Loading full text...

Full text loading...

/deliver/fulltext/jgv/72/9/JV0720092311.html?itemId=/content/journal/jgv/10.1099/0022-1317-72-9-2311&mimeType=html&fmt=ahah

References

  1. Brown S. M., Harland J. 1987; Three mutants of herpes simplex virus type 2: one lacking the genes US10, US11 and US12 and two in which RS has been extended by 6 kb to 0.91 map units with loss of US sequences between 0.94 and the US/TRS junction. Journal of General Virology 68:1–18
    [Google Scholar]
  2. Harland J., Brown S. M. 1985; Isolation and characterization of deletion mutants of herpes simplex virus type 2 (strain HG52). Journal of General Virology 66:1305–1321
    [Google Scholar]
  3. McGeoch D. J. 1984; The nature of animal virus genetic material. In The Microbe 1984, Part I: Viruses pp 75–107 Edited by Mahy B. W. J., Pattison J. R. Cambridge: Cambridge University Press;
    [Google Scholar]
  4. Mclean A. R., Brown S. M. 1987; Deletion and duplication variants around the long repeats of herpes simplex virus type 1 strain 17. Journal of General Virology 68:3019–3031
    [Google Scholar]
  5. Maniatis T., Fritsch E. F., Sambrook J. 1982 Molecular Cloning: A Laboratory Manual New York: Cold Spring Harbor Laboratory:
    [Google Scholar]
  6. Mitchell W. J., Steiner I., Brown S. M., MacLean A. R., Subak-Sharpe J. H., Fraser N. W. 1990; A herpes simplex virus type 1 variant, deleted in the promoter region of the latency-associated transcripts, does not produce any detectable minor RNA species during latency in the mouse trigeminal ganglion. Journal of General Virology 71:953–957
    [Google Scholar]
  7. Perry L. J., McGeoch D. J. 1988; The DNA sequences of the long repeat region and adjoining parts of the long unique region in the genome of herpes simplex virus type 1. Journal of General Virology 69:2831–2846
    [Google Scholar]
  8. Sacks W. R., Greene C. C., Aschmann D. P., Schaffer P. A. 1985; Herpes simplex virus type 1 ICP27 is an essential regulatory protein. Journal of Virology 55:796–805
    [Google Scholar]
  9. Sanger F., Nicklen S., Coulson A. R. 1977; DNA sequencing with chain-terminating inhibitors. Proceedings of the National Academy of Sciences, U.S.A 74:5463–5467
    [Google Scholar]
  10. Sanger F., Coulson A. R., Barrell B. G., Smith A. J. H., Roe B. A. 1980; Cloning in single-stranded bacteriophage as an aid to rapid DNA sequencing. Journal of Molecular Biology 143:161–178
    [Google Scholar]
  11. Southern E. M. 1975; Detection of specific sequences among DNA fragments separated by gel electrophoresis. Journal of Molecular Biology 98:503–517
    [Google Scholar]
  12. Spivack J. G., Fraser N. W. 1987; Detection of herpes simplex virus type 1 transcripts during latent infection in mice. Journal of Virology 61:3841–3847
    [Google Scholar]
  13. Steiner I., Spivack J. G., Lirette R. P., Brown S. M., MacLean A. R., Subak-Sharpe J. H., Fraser N. W. 1989; Herpes simplex virus type 1 latency-associated transcripts are evidently not essential for latent infection. EMBO Journal 8:505–511
    [Google Scholar]
  14. Stevens J. G., Wagner E. K., Devi-Rao G. B., Cook M. L., Feldman L. T. 1987; RNA complementary to a herpes virus alpha gene mRNA is prominent in latently infected neurons. Science 235:1056–1059
    [Google Scholar]
  15. Weschler S. L., Nesburn A. B., Watson R., Slanina S. M., Ghiasi H. 1988; Fine mapping of the latency-related gene of herpes simplex virus type 1: alternative splicing produces distinct latency-related RNAs containing open reading frames. Journal of Virology 62:4051–4058
    [Google Scholar]
  16. Whitton J. L., Clements J. B. 1984; The junctions between the repetitive and the short unique sequences of the herpes simplex virus genome are determined by the polypeptide-coding regions of two spliced immediate-early mRNAs. Journal of General Virology 65:451–466
    [Google Scholar]
http://instance.metastore.ingenta.com/content/journal/jgv/10.1099/0022-1317-72-9-2311
Loading
/content/journal/jgv/10.1099/0022-1317-72-9-2311
Loading

Data & Media loading...

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error