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High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing
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High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing

Published on: January 22, 2019

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HIV Transcription Is Independent of Mediator Kinases

Daniele C Cary1, Mona Rheinberger1, Ajda Rojc1

  • 1Department of Medicine, University of California at San Francisco, San Francisco, California.

AIDS Research and Human Retroviruses
|May 3, 2019
PubMed

Insights

Mediator kinases (MDKs), including CDK8 and CDK19, do not play a role in HIV transcription. Studies show that inhibiting or reducing MDKs does not affect HIV gene expression or viral reactivation from latency.

Area of Science:

  • Molecular Biology
  • Virology
  • Gene Regulation

Background:

  • Cyclin-dependent kinases (CDKs) are crucial for HIV transcription, but the roles of mediator kinases (MDKs) like CDK8 and CDK19 remain unclear.
  • Mediator complexes, which include MDKs, are known to modulate gene expression, potentially impacting viral processes.
  • Understanding MDK involvement is key to comprehending the full spectrum of host factors regulating HIV.

Purpose of the Study:

  • To investigate the specific role of mediator kinases (MDKs), namely CDK8 and CDK19, in the process of HIV transcription.
  • To determine if MDKs are essential for the expression of HIV genes.
  • To assess the potential of MDK inhibitors as a strategy to control HIV replication or reactivation.

Main Methods:

  • Utilized small interfering RNA (siRNA) to specifically reduce the levels of CDK8 and CDK19.
  • Employed chemical inhibitors, Cortistatin A (CA) and Senexin A (SnxA), known to target MDKs.
  • Assessed HIV transcription levels and viral reactivation in Jurkat cell models of HIV latency.

Main Results:

  • siRNA-mediated knockdown of both CDK8 and CDK19 did not significantly alter HIV transcription.
  • Treatment with MDK inhibitors Cortistatin A and Senexin A failed to inhibit HIV transcription.
  • Neither Cortistatin A nor Senexin A demonstrated efficacy in blocking viral reactivation from latency in Jurkat cells.

Conclusions:

  • Mediator kinases (MDKs), CDK8 and CDK19, are not required for HIV transcription.
  • Targeting MDKs with inhibitors like CA and SnxA is not an effective strategy for inhibiting HIV gene expression or reactivation from latency.
  • These findings exclude MDKs from the essential host factors governing HIV transcription and replication.
Keywords:
CDK19CDK8Cortistatin AHIV transcriptionSenexin Amediator kinases

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