Sunlight induced progression of AIDS

Med Hypotheses. 1995 Feb;44(2):119-23. doi: 10.1016/0306-9877(95)90083-7.

Abstract

Ultraviolet B (UVB) radiation in sunlight damages the cutaneous immune system of individuals primarily by converting trans-urocanic acid (UCA) to its cis isoform which in turn instigates excessive local, and eventually systemic, levels of tumor necrosis factor-alpha (TNF alpha). UVB radiation and TNF alpha have been found to activate HIV from the latent state, and TNF alpha has been implicated in the pathogenesis of several manifestations of the acquired immune deficiency syndrome (AIDS). We hypothesize that the immunosuppressant properties of TNF alpha and cis-UCA, released by intense sun exposure, can accelerate the onset and progression of AIDS in HIV-infected individuals.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acquired Immunodeficiency Syndrome / physiopathology*
  • Animals
  • Disease Progression
  • Epidermis / immunology*
  • Epidermis / radiation effects
  • HIV / growth & development
  • Humans
  • Immune Tolerance / radiation effects
  • Immunocompetence / radiation effects
  • Mice
  • Models, Immunological
  • Prostaglandins E / biosynthesis
  • Sunlight / adverse effects*
  • Th2 Cells / immunology
  • Tumor Necrosis Factor-alpha / metabolism*
  • Ultraviolet Rays / adverse effects*
  • Urocanic Acid / radiation effects
  • Virus Activation

Substances

  • Prostaglandins E
  • Tumor Necrosis Factor-alpha
  • Urocanic Acid