Classically, Reiter's syndrome was defined as a triad of arthritis, ur
ethritis, and conjunctivitis. In 1981, the American Rheumatism Associa
tion revised its defining criteria for Reiter's syndrome as an episode
of peripheral arthritis of more than 1 month's duration occurring in
association with urethritis and/or cervicitis. Reiter's syndrome is al
so associated with mucocutaneous lesions. Reiter's syndrome was first
described in association with the human immunodeficiency virus (HIV) i
n 1987. The course of Reiter's syndrome in HIV is more severe, progres
sive, and refractory to treatment than in non-HIV-positive patients. T
he immunopathogenesis of Reiter's syndrome is linked to HLA-B27, which
has been described as the disease susceptibility factor. The associat
ion of Reiter's syndrome and HLA-B27 positivity is 80%. Infectious age
nts may play a critical role in the initiation or perpetuation of Reit
er's syndrome. It has been suggested that an amino acid sequence withi
n the HLA-B27 molecule allows microbial peptides to bind and be presen
ted to T cytotoxic cells (CD8), which results in a primary T cytotoxic
cell response against various tissues. The role of the HIV in the pat
hogenesis of Reiter's syndrome is still being investigated. Human immu
nodeficiency virus may directly cause arthritis, it may increase the h
ost's susceptibility to infection with arthritogenic organisms. Additi
onally, HIV infection increases the relative number of CD8 cells, whic
h may play a key role in the pathogenesis of Reiter's syndrome. In thi
s article, we present a case of Reiter's syndrome in an HLA-B27 and HI
V-positive patient, and a review of the literature on the infectious,
immunologic, and dermatologic aspects of Reiter's syndrome in HIV dise
ase.