The mechanism underlying a transition of the oral cavity mucosal epithelium
towards susceptibility to opportunistic infections in HIV-seropositive pat
ients was investigated, Phenotypic markers CD1a, HLA-DR, and CD86 of oral m
ucosal Langerhans' cells (LCs), p17 core protein of human immunodeficiency
virus (HIV), and CD45RO of memory T cells were labeled on oral hairy leukop
lakia lesional biopsies and clinically normal autologous tissue of HIV-infe
cted patients. HIV p17 protein was detected in association with mucosal LCs
, mainly within the lesional epithelium. There were significant correlation
s between the detection of HIV p17 and the depletion of LCs, and between th
e depletion of LCs and the presence of hairy leukoplakia lesions. Conjugate
s of activated LCs and memory T cells were also evident in the submucosal a
rea of lesional biopsies. The findings from this study support the hypothes
is that oral mucosal LCs are also the target of HIV infection. Cytopathic c
hanges of LCs caused by productive HIV infection may contribute to selectiv
e depletion of LCs, which may impair the mucosal immunologic protection aga
inst colonization by microorganisms causing HIV-associated oral mucosal les
ions.