Oral candidiasis caused by Candida albicans is recognized as one of the most frequent opportunistic infections in human immunodeficiency virus (HIV)-infected individuals. The overall severity and chronicity of oral candidiasis has been attributed exclusively to the HIV-induced immune deficiency of the affected individuals but not to the virulence factors of the pathogen, i.e. C. albicans. However, genotypic and phenotypic studies have suggested that HIV infection might be associated with preferential selection of C. albicans strains with altered virulence determinants, leading to colonization with Candida populations that are better able to cause disease in these immunologically compromised hosts. If this process of selection is indeed related to pathogenicity, it may be possible to measure alterations in different virulence factors produced by C. albicans in HIV-infected patients. To evaluate this hypothesis, the present work was undertaken to determine simultaneously the expression of five virulence factors in oral C. albicans isolates colonizing and infecting HIV-positive and -negative individuals. The significance of genotypes in the pathogenesis of oral candidiasis was also elucidated. Oral swabs were collected from 335 consecutive individuals (210 HIV-positive and 125 HIV-negative). Virulence factors and genotypes were determined for all the C. albicans strains isolated. The results showed significantly increased expression of proteinase, phospholipase and haemolytic activities, as well as a greater ability to adhere, in isolates from HIV-positive compared with HIV-negative individuals (P<0.05). However, no significant differences in virulence factor expression in isolates colonizing or infecting HIV-positive individuals were seen. Genotype A was the predominant type (71.3 %); however, a relationship could not be established between the genotypes and the virulence factors, or with clinical infection. These data support the concept of preferential C. albicans strain selection with altered virulence determinants in HIV-infected individuals and emphasize the need for further molecular genetic linkage studies that could be helpful in dissecting the molecular causes of preferential strain selection, which may lead to new approaches for therapeutic intervention.