PURPOSE: To morphometrically quantify CD1a+ dentritic cells and DC-SIGN+ 
dendritic cells in HIV-positive patients with anal squamous intraepithelial 
neoplasia and to evaluate the effects of HIV infection, antiretroviral therapy 
and HPV infection on epithelial and subepithelial dendritic cells.
METHODS: A prospective study was performed to morphometrically analyze the 
relative volume of the dendritic cells and the relationship between anal 
intraepithelial neoplasia and cancer in HIV-positive patients from the Tropical 
Medicine Foundation of Amazonas, Brazil. All patients were submitted to biopsies 
of anorectal mucosa to perform a classic histopathological and 
immunohistochemical analysis, employing antibodies against CD1a and DC-SIGN for 
the morphometric quantification of dendritic cells.
RESULTS: HIV-negative patients displayed a CD1a DC density significantly higher 
than that of HIV-positives patients (3.75 versus 2.54) (p=0.018), and in 
patients with severe anal intraepithelial neoplasia had correlated between DC 
CD1a density with levels of CD4 + cells (p: 0.04) as well as the viral load of 
HIV-1 (p: 0.035). A not significant rise in the median density of CD1a+ DC was 
observed in the HIV positive/ HAART positive subgroup compared to the HIV 
positive/ HAART negative subgroup. The CD1a+ DC were also significantly 
increased in HIV-negative patients with anorectal condyloma (2.33 to 3.53; 
p=0.05), with an opposite effect in HIV-positive patients.
CONCLUSIONS: Our data support an enhancement of the synergistic action caused by 
HIV-HPV co-infection on the anal epithelium, weakening the DC for its major role 
in immune surveillance. Notoriously in patients with severe anal intraepithelial 
neoplasia, the density of CD1a+ epithelial dendritic cells was influenced by the 
viral load of HIV-1. Our study describes for the first time the density of 
subepithelial DC-SIGN+ dendritic cells in patients with anal severe anal 
intraepithelial neoplasia and points to the possibility that a specific therapy 
for HIV induces the recovery of the density of epithelial DC.