Oropharyngeal Candidiasis, Candida Albicans Infections, and Oral Immune Mediators Associated with Oral Human Immunodeficiency Virus: A Literature Review
{"title":"Oropharyngeal Candidiasis, Candida Albicans Infections, and Oral Immune Mediators Associated with Oral Human Immunodeficiency Virus: A Literature Review","authors":"Cameron B.R. King","doi":"10.26685/urncst.563","DOIUrl":null,"url":null,"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.","PeriodicalId":245521,"journal":{"name":"Undergraduate Research in Natural and Clinical Science and Technology (URNCST) Journal","volume":" 33","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Undergraduate Research in Natural and Clinical Science and Technology (URNCST) Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.26685/urncst.563","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
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.
介绍:虽然白色念珠菌通常是共生菌,在健康人的口腔中存在密度较低,但免疫系统受损会导致这种真菌过度生长,导致口腔微生物组 "菌群失调 "和免疫反应激活。在严重的情况下,白色念珠菌过度生长会导致口腔感染,称为口咽念珠菌病(OPC),与口腔炎症、病变和溃疡有关。虽然人类免疫缺陷病毒(HIV)感染与口咽念珠菌病的风险增加有关,但很少有研究将口咽念珠菌病和白僵菌感染与随后的口腔 HIV 感染风险联系起来。有关口腔微生物组及其如何改变 HIV 风险的证据也很缺乏。研究方法在 PubMed、Google Scholar 和阿尔伯塔大学图书馆数据库(University of Alberta Library Database)上进行了文献检索,时间从开始到 2023 年 11 月。结果与讨论:口腔传播艾滋病毒的风险很低。通过激活与清除微生物病原体相关的免疫反应、诱导炎症和与 HIV 风险相关的细胞因子(包括 IL-17、IL-6 和 IL-1ß)的升高,OPC 和白僵菌真菌感染可增加对 HIV 的易感性。持续的白念珠菌感染还会促进 Thelper 17 细胞(T-helper 17 细胞是常见的 HIV 靶细胞)和中性粒细胞的招募,中性粒细胞会在炎症时释放中性粒细胞蛋白酶,并介导紧密连接蛋白的裂解,最终破坏口腔微生物群。结论免疫细胞招募到粘膜的增加和上皮细胞破坏的增加可能会促进艾滋病毒病毒穿过上皮细胞扩散并进入免疫靶细胞,这表明 OPC 和白念珠菌感染有可能增加口腔感染艾滋病毒的风险。有关白僵菌密度、OPC 和口腔 HIV 风险之间关系的证据有限,因此今后需要进行高质量的横断面研究。