Lost in transcription: Molecular mechanisms that control HIV latency

Ran Taube, Boris Matija Peterlin

Research output: Contribution to journalArticlepeer-review

56 Scopus citations


Highly active antiretroviral therapy (HAART) has limited the replication and spread of the human immunodeficiency virus (HIV). However, despite treatment, HIV infection persists in latently infected reservoirs, and once therapy is interrupted, viral replication rebounds quickly. Extensive efforts are being directed at eliminating these cell reservoirs. This feat can be achieved by reactivating latent HIV while administering drugs that prevent new rounds of infection and allow the immune system to clear the virus. However, current approaches to HIV eradication have not been effective. Moreover, as HIV latency is multifactorial, the significance of each of its molecular mechanisms is still under debate. Among these, transcriptional repression as a result of reduced levels and activity of the positive transcription elongation factor b (P-TEFb: CDK9/cyclin T) plays a significant role. Therefore, increasing levels of P-TEFb expression and activity is an excellent strategy to stimulate viral gene expression. This review summarizes the multiple steps that cause HIV to enter into latency. It positions the interplay between transcriptionally active and inactive host transcriptional activators and their viral partner Tat as valid targets for the development of new strategies to reactivate latent viral gene expression and eradicate HIV.

Original languageEnglish
Pages (from-to)902-927
Number of pages26
Issue number3
StatePublished - 21 Mar 2013


  • Epigenetic
  • HIV latency
  • Positive transcription elongation factor b (P-TEFb)
  • Tat
  • Transcriptional interference

ASJC Scopus subject areas

  • Infectious Diseases
  • Virology


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