Ultraviolet irradiation and cytokines as regulators of HIV latency and expression.
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.
Vicenzi
E
E
AIDS Immunopathogenesis Unit, San Raffaele Hospital, Centro San Luigi, Milan, Italy.
Poli
G
G
D000818:Animals; D016207:Cytokines / Q000494:pharmacology / Q000502:physiology*; D015967:Gene Expression Regulation, Viral / Q000187:drug effects / Q000528:radiation effects; D006678:HIV / Q000187:drug effects / Q000235:genetics / Q000502:physiology* / Q000528:radiation effects; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D016328:NF-kappa B / Q000378:metabolism; D014466:Ultraviolet Rays; D015854:Up-Regulation; D014775:Virus Activation / Q000187:drug effects / Q000528:radiation effects; D017735:Virus Latency / Q000187:drug effects / Q000528:radiation effects; D014779:Virus Replication / Q000187:drug effects / Q000528:radiation effects
D016207:Cytokines; D016328:NF-kappa B