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Selection and pathogenicity of Candida albicans in HIV infection.

The progression of immune-suppression due to infection with HIV is mirrored by an increase in the severity and prevalence of oral candidosis. The transition of C. albicans from harmless commensal to unrelenting pathogen in the susceptible host is a fine line attributable to an extensive repertoire of selectively expressed virulence determinants, including hyphal formation, thigmotropism, protease secretion, adherence and phenotypic switching. The transition from commensal to pathogen has been linked to the formation of elongated hyphae which may more readily penetrate epithelial surfaces. Invasion may be enhanced by thigmotropism which enables hyphae to sense intercellular junctions and surface discontinuities in order to find areas that may be more readily breached. Electron micrograph studies suggest that C. albicans are able to penetrate mucosal tissues by secreting hydrolytic enzymes at the tip of the invading hyphae. Recent studies have shown that protease secretion is upregulated in C. albicans isolated from AIDS patients. Similarly, the propensity for C. albicans to adhere to oral mucosa appears to be enhanced in isolates from HIV-infected subjects. These two virulence determinants may be coordinately regulated and DNA fingerprinting studies suggest that these phenotypic alterations may be associated with the selection of C. albicans with altered genotypes. The mechanisms by which hypervirulent C. albicans may be selected in HIV-infected patients is likely to be a multifactorial process associated with the pathobiological effects of HIV infection and to the increased candidal proliferation so evident in these patients.