NF-κB sub-pathways and HIV cure: A revisit

EBioMedicine. 2021 Jan:63:103159. doi: 10.1016/j.ebiom.2020.103159. Epub 2020 Dec 16.


HIV cure is thwarted by the presence of quiescent yet replication competent HIV-1 (HIV). Antiretroviral therapy (ART) is unable to eradicate reservoirs, and upon cessation of ART, HIV will rebound. This review encompasses the curative strategies of HIV in the context of NF-κB sub-pathways that are currently exploited and demonstrate promise in the disruption of latent HIV. Canonical NF-κB signaling has long been established to drive HIV proviral expression while noncanonical NF-κB signaling, a novel and perhaps more desirable mechanism of latency reversal due to its unique characteristics, has recently been shown to also promote HIV expression from latency. Furthermore, we discuss the previously unrecognized upstream signaling of NF-κB as a new avenue for exploration of a functional cure of HIV.

Keywords: Canonical NF-κB; HIV cure; HIV latency; Noncanonical NF-κB; PEBP1; Raf1.

Publication types

  • Review

MeSH terms

  • Animals
  • Anti-HIV Agents / chemistry
  • Anti-HIV Agents / pharmacology
  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / metabolism
  • CD4-Positive T-Lymphocytes / virology
  • Drug Discovery
  • Gene Expression Regulation, Viral
  • HIV / drug effects
  • HIV / physiology*
  • HIV Infections / drug therapy
  • HIV Infections / metabolism*
  • HIV Infections / virology*
  • Host-Pathogen Interactions*
  • Humans
  • NF-kappa B / metabolism*
  • Protein Kinase C / metabolism
  • Signal Transduction* / drug effects
  • Virus Latency / drug effects
  • Virus Latency / genetics
  • Virus Replication


  • Anti-HIV Agents
  • NF-kappa B
  • Protein Kinase C