Abstract

Introduction: While Candida albicans are usually commensal and present in low density in the oral cavity of healthy individuals, an immunocompromised immune system can lead to the overgrowth of this fungal species, leading to oral microbiome “dysbiosis” and activation of immune responses. In severe cases, C. albicans overgrowth can lead to an oral infection called oropharyngeal candidiasis (OPC), which is associated with inflammation, lesions, and sores of the oral cavity. While human immunodeficiency virus (HIV) infection has been linked to an increased risk of OPC, few studies have associated OPC and C. albicans infection with subsequent risk for oral HIV acquisition. Evidence on the oral microbiome and how it can alter HIV risk is also lacking. Methods: A literature search was performed on PubMed, Google Scholar, and the University of Alberta Library Database from inception to November 2023. Results and Discussion: The risk of oral HIV transmission is low. OPC and C. albicans fungal infection can increase HIV susceptibility by activating immune responses associated with the clearance of microbial pathogens, inducing inflammation and elevations in cytokines related to HIV risk including IL-17, IL-6 and IL-1ß. Persistent C. albicans infections also promote the recruitment of T-helper 17 cells, which is a common HIV target cell, and neutrophils, which releases neutrophil proteases upon inflammation and mediates the cleavage of tight junction proteins, ultimately disrupting the oral microbiome. Conclusion: Increased immune cell recruitment to the mucosa and increased epithelial breakdown may facilitate the diffusion and access of HIV virions across the epithelium to immune target cells, suggesting that OPC and C.albicans infections has the potential to increase risk for oral HIV acquisition. Limited evidence of the relationship between C. albicans density, OPC, and oral HIV risk, warrants high-quality cross-sectional studies in the future.

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