人类免疫缺陷病毒相关的微生物易位与丙型肝炎的进展
Human immunodeficiency virus-related microbial translocation and progression of hepatitis C.
作者信息
Balagopal Ashwin, Philp Frances H, Astemborski Jacquie, Block Timothy M, Mehta Anand, Long Ronald, Kirk Gregory D, Mehta Shruti H, Cox Andrea L, Thomas David L, Ray Stuart C
机构信息
Division of Infectious Diseases, Viral Hepatitis Center, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
出版信息
Gastroenterology. 2008 Jul;135(1):226-33. doi: 10.1053/j.gastro.2008.03.022. Epub 2008 Mar 29.
BACKGROUND & AIMS: Human immunodeficiency virus (HIV)-1 infection has been associated with enhanced microbial translocation, and microbial translocation is a mechanism through which alcohol and some enteric conditions cause liver disease. We hypothesized that HIV promotes liver disease by enhancing microbial translocation.
METHODS
We studied human cohorts in which hepatitis C virus (HCV) and HIV outcomes were carefully characterized.
RESULTS
HIV-related CD4(+) lymphocyte depletion was strongly associated with microbial translocation as indicated by elevated levels of circulating lipopolysaccharide (LPS), LPS-binding protein, soluble CD14, and fucose-binding lectin (AAL) reactive to immunoglobulin G specific for the alpha-galactose epitope and suppressed levels of endotoxin core antibodies (EndoCAb IgM) in HIV-infected subjects compared with the same persons before they had HIV infection and compared with HIV-uninfected subjects. The same measures of microbial translocation were strongly associated with HCV-related liver disease progression (cirrhosis), eg, LPS, odds ratio, 19.0 (P = .002); AAL, odds ratio, 27.8 (P < .0001); in addition, levels of LPS were elevated prior to recognition of cirrhosis.
CONCLUSIONS
Microbial translocation may be a fundamental mechanism through which HIV accelerates progression of chronic liver disease.
背景与目的
人类免疫缺陷病毒1型（HIV-1）感染与微生物易位增强有关，而微生物易位是酒精和某些肠道疾病导致肝病的一种机制。我们推测HIV通过增强微生物易位促进肝病发生。
方法
我们研究了仔细界定了丙型肝炎病毒（HCV）和HIV结局的人类队列。
结果
与感染HIV之前的同一人群以及未感染HIV的受试者相比，HIV相关的CD4(+)淋巴细胞耗竭与微生物易位密切相关，这表现为HIV感染受试者循环脂多糖（LPS）、LPS结合蛋白、可溶性CD14以及对α-半乳糖表位特异性免疫球蛋白G有反应的岩藻糖结合凝集素（AAL）水平升高，以及内毒素核心抗体（EndoCAb IgM）水平降低。微生物易位的相同指标与HCV相关的肝病进展（肝硬化）密切相关，例如，LPS的比值比为19.0（P = .002）；AAL的比值比为27.8（P < .0001）；此外，在诊断出肝硬化之前LPS水平就已升高。
结论
微生物易位可能是HIV加速慢性肝病进展的一种基本机制。
Zotero 插件