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首页> 外文期刊>AIDS >Candida and candidiasis in HIV-infected patients: Where commensalism, opportunistic behavior and frank pathogenicity lose their borders
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Candida and candidiasis in HIV-infected patients: Where commensalism, opportunistic behavior and frank pathogenicity lose their borders

机译：HIV感染患者中的念珠菌和念珠菌病：共情，机会主义行为和坦率的致病性使人无法接受

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摘要

In this era of efficacious antiretroviral therapy and consequent immune reconstitution, oropharyngeal and esophageal candidiasis (OPC and OEC) still remain two clinically relevant presentations in the global HIV setting. Both diseases are predominantly caused by Candida albicans, a polymorphic fungus which is a commensal microbe in the healthy individual but can become an aggressive pathogen in a debilitated host. Actually, C. albicans commensalism is not the result of a benign behavior of one of the many components of human microbiota, but rather the result of host's potent innate and adaptive immune responses that restrict the growth of a potentially dangerous microrganism on the epithelia. An important asset guarding against the fungus is the Th17 functional subset of T helper cells. The selective loss of these cells with the progression of HIV infection causes the decay of fungal containment on the oral epithelium and allows C. albicans to express its pathogenic potential. An important part of this potential is represented by mechanisms to evade host immunity and enhance inflammation and immunoactivation. In C. albicans, these mechanisms are mostly incorporated into and expressed by characteristic morphogenic transitions such as the yeast-to-hyphal growth and the white-to-opaque switch. In addition, HIV infection generates an 'environment' selecting for overexpression of the virulence potential by the fungus, particularly concerning the secreted aspartyl proteinases (Saps). These enzymes can degrade critical host defense components such as complement and epithelial defensive proteins such as histatin-5 and E-cadherin. It appears that part of this enhanced Candida virulence could be induced by the binding of the fungus to HIV and/or induced by HIV proteins such as GP160 and tat. Both OPC and OEC can be controlled by old and new antimycotics, but in the absence of host collaboration, anticandidal therapy may become ineffective in the long run. For these reasons, new therapeutics targeting virulence factors and specific immune interventions are being addressed. Among these new approaches, vaccination is a promising one. Two subunit vaccines based on antigens dominantly expressed by C. albicans in vivo, that is the Als3 adhesin and Sap2, have recently undergone phase 1 clinical trials. Overall, studies of Candida and candidiasis in the HIV-positive patient while certainly contributing to a more effective control of the microorganism may also provide useful information on HIV-host relationship itself that can assist the fight against the virus.
机译：在这个有效的抗逆转录病毒疗法和随之而来的免疫重建的时代，口咽和食管念珠菌病（OPC和OEC）仍然是全球HIV设置中两个临床相关的表现。两种疾病主要是由白色念珠菌引起的。白色念珠菌是一种多态性真菌，在健康个体中是共生微生物，但在衰弱的宿主中可能成为侵袭性病原体。实际上，白色念珠菌的共鸣不是人类微生物群许多组成部分之一的良性行为的结果，而是宿主强大的先天性和适应性免疫反应的结果，这种免疫反应限制了潜在危险的微生物在上皮细胞上的生长。防御真菌的重要资产是T辅助细胞的Th17功能子集。随着HIV感染的进展，这些细胞的选择性丢失会导致口腔上皮的真菌抑制作用减弱，并使白色念珠菌表达其致病潜能。这种潜力的重要组成部分是逃避宿主免疫力，增强炎症和免疫激活的机制。在白色念珠菌中，这些机制大部分被并入特征性形态发生转变中，并由其表达，例如酵母菌丝到菌丝的生长以及白色菌丝到不透明的菌丝。此外，HIV感染会产生一个“环境”，以选择真菌过度表达潜在的毒力，特别是涉及分泌的天冬氨酰蛋白酶（Saps）。这些酶可以降解关键的宿主防御成分，例如补体和上皮防御蛋白，例如histatin-5和E-cadherin。看来，这种增强的念珠菌毒力的一部分可以由真菌与HIV的结合诱导和/或由HIV蛋白（如GP160和tat）诱导。 OPC和OEC均可受新旧抗真菌药的控制，但是在没有宿主协作的情况下，从长远来看，抗念珠菌疗法可能会失效。由于这些原因，针对毒力因子和特异性免疫干预的新疗法正在被研究。在这些新方法中，疫苗接种是一种有前途的方法。最近有两种基于白色念珠菌在体内主要表达的抗原的亚单位疫苗，即Als3粘附素和Sap2，已进行了1期临床试验。总体而言，对HIV阳性患者进行念珠菌和念珠菌病的研究虽然肯定有助于更有效地控制微生物，但也可能提供有关HIV宿主关系本身的有用信息，有助于抗击病毒。

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