The gene that encodes the herpes simplex virus type 1 latency-associated transcript influences the accumulation of transcripts (Bcl-x(L) and Bcl-x(S)) that encode apoptotic regulatory proteins

J Virol. 2003 Oct;77(19):10714-8. doi: 10.1128/jvi.77.19.10714-10718.2003.

Abstract

The herpes simplex virus type 1 latency-associated transcript (LAT) inhibits apoptosis. We demonstrate here that LAT influences the accumulation of the Bcl-x(L) transcript versus the Bcl-x(S) transcript in Neuro-2A cells. Bcl-x(L) encodes an antiapoptotic protein, whereas Bcl-x(S) encodes a proapoptotic protein. Promoting the accumulation of Bcl-x(L) in neurons may inhibit apoptosis, thus enhancing the latency-reactivation cycle.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Apoptosis*
  • Herpesvirus 1, Human / genetics*
  • Humans
  • MicroRNAs
  • Proto-Oncogene Proteins c-bcl-2 / genetics*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Cells, Cultured
  • Viral Proteins / genetics*
  • Virus Latency
  • bcl-X Protein

Substances

  • BCL2L1 protein, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger
  • Viral Proteins
  • bcl-X Protein
  • latency associated transcript, herpes simplex virus-1