Ultraviolet irradiation and cytokines as regulators of HIV latency and expression

Chem Biol Interact. 1994 Jun;91(2-3):101-9. doi: 10.1016/0009-2797(94)90030-2.


The ability of the human immunodeficiency virus (HIV) to persist and replicate in human CD4+ T lymphocytes and mononuclear phagocytes is under the control of both virally encoded proteins and a variety of host-related factors. Ultraviolet (UV) light has been shown to induce transcription and expression of HIV. Both DNA damage and repair and DNA damage/repair-independent pathways caused by UV irradiation lead to expression of proviral HIV genomes via activation of the cellular transcription factor NF-kappa B. Transgenic mice that contain either long terminal repeat (LTR)-reporter genes or HIV genomes, either full length or deleted in the gag-pol region, express RNA and proteins at the epidermal level, particularly after UV irradiation. Furthermore, UV-triggered release of soluble factors capable of inducing expression of HIV in non-irradiated cells has been observed. Among other host factors, the functional network of pro-inflammatory and immunoregulatory cytokines has been demonstrated to act as a potent regulator of HIV replication, at least in different in vitro systems of infection.

Publication types

  • Review

MeSH terms

  • Animals
  • Cytokines / pharmacology
  • Cytokines / physiology*
  • Gene Expression Regulation, Viral / drug effects
  • Gene Expression Regulation, Viral / radiation effects
  • HIV / drug effects
  • HIV / genetics
  • HIV / physiology*
  • HIV / radiation effects
  • Humans
  • Mice
  • Mice, Transgenic
  • NF-kappa B / metabolism
  • Ultraviolet Rays*
  • Up-Regulation
  • Virus Activation / drug effects
  • Virus Activation / radiation effects
  • Virus Latency* / drug effects
  • Virus Latency* / radiation effects
  • Virus Replication / drug effects
  • Virus Replication / radiation effects


  • Cytokines
  • NF-kappa B