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