Lung microbiome in human immunodeficiency virus infection

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• 作者：Homer L. Twigg III^a ; ^htwig@iu.edu ; George M. Weinstock^b ; Kenneth S. Knox^c
• 关键词：NIH ; National Institutes of Health ; HIV ; human immunodeficiency virus ; LHMP ; Lung Human Microbiome Project ; ART ; antiretroviral therapy ; AM ; alveolar macrophage ; BAL ; bronchoalveolar lavage ; COPD ; chronic obstructive lung disease ; OTU ; operational taxonomic unit ; DNA ; deoxyribonucleic acid ; RNA ; ribonucleic acid ; PBMCs ; peripheral blood mononuclear cells
• 刊名：Translational Research
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：179
• 期：Complete
• 页码：97-107
• 全文大小：715 K
• 卷排序：179

文摘

The lung microbiome plays a significant role in normal lung function and disease. Because microbial colonization is likely influenced by immunodeficiency, one would speculate that infection with human immunodeficiency virus (HIV) alters the lung microbiome. Furthermore, how this alteration might impact pulmonary complications now seen in HIV-infected patients on antiretroviral therapy (ART), which has shifted from opportunistic infections to diseases associated with chronic inflammation, is not known. There have been limited publications on the lung microbiome in HIV infection, many of them emanating from the Lung HIV Microbiome Project. Current evidence suggests that the lung microbiome in healthy HIV-infected individuals with preserved CD4 counts is similar to uninfected individuals. However, in individuals with more advanced disease, there is an altered alveolar microbiome characterized by a loss of richness and evenness (alpha diversity) within individuals. Furthermore, as a group the taxa making up the HIV-infected and uninfected lung microbiome are different (differences in beta diversity), and the HIV-infected population is more spread out (greater dispersion) than the uninfected population. These differences decline with ART, but even after effective therapy the alveolar microbiome in HIV-infected individuals contains increased amounts of signature bacteria, some of which have previously been associated with chronic lung inflammation. Furthermore, more recent investigations into the lung virome in HIV infection suggest that perturbations in lung viral communities also exist in HIV infection, and that these too are associated with evidence of lung inflammation. Thus, it is likely both microbiome and virome alterations in HIV infection contribute to lung inflammation in these individuals, which has important implications on the changing spectrum of pulmonary complications in patients living with HIV.