The HSV-1 latency associated transcript (LAT) variants 1704 and 1705 are glycoprotein C negative

Zofia Wroblewska, Jordan G. Spivack, Jessica Otte, Israel Steiner, Moira Brown, Alasdair MacLean, Nigel W. Fraser

Research output: Contribution to journalArticlepeer-review

Abstract

The latency associated transcripts (LAT) of herpes simplex virus type 1 (HSV-1) are encoded by diploid genes that are expressed during latent infections. Two LAT variant viruses, 1704 and 1705, were compared with the parental strain 17+. Variant 1705 has a deletion affecting one copy of the LAT genes, expresses LATs during latent infection and reactivates normally. Variant 1704 has deletions affecting both LAT gene copies, does not express LATs during latent infection, and its reactivation is impaired (Steiner et al., 1989). Comparison of infected cell proteins by immunoprecipitation and Western blot analysis revealed one significant difference between HSV-1 strain 17+, 1704 and 1705; glycoprotein C (gC) was not synthesized by 1704 or 1705. Since both 1704 and 1705 are gC minus, the reactivation defect of 1704 is most likely related to the absence of the LATs, and not to the absence of gC.

Original languageEnglish
Pages (from-to)193-200
Number of pages8
JournalVirus Research
Volume20
Issue number2
DOIs
StatePublished - Jul 1991
Externally publishedYes

Keywords

  • Herpes simplex virus type 1
  • Latency associated transcript
  • Latent infection

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