Guadalupe Moraima, Sankaran Sumathi, George Michael D, Reay Elizabeth, Verhoeven David, Shacklett Barbara L, Flamm Jason, Wegelin Jacob, Prindiville Thomas, Dandekar Satya
Dept. of Medical Microbiology and Immunology, GBSF, Room 5511, University of California, Davis, CA 95616, USA.
J Virol. 2006 Aug;80(16):8236-47. doi: 10.1128/JVI.00120-06.
Although the gut-associated lymphoid tissue (GALT) is an important early site for human immunodeficiency virus (HIV) replication and severe CD4+ T-cell depletion, our understanding is limited about the restoration of the gut mucosal immune system during highly active antiretroviral therapy (HAART). We evaluated the kinetics of viral suppression, CD4+ T-cell restoration, gene expression, and HIV-specific CD8+ T-cell responses in longitudinal gastrointestinal biopsy and peripheral blood samples from patients initiating HAART during primary HIV infection (PHI) or chronic HIV infection (CHI) using flow cytometry, real-time PCR, and DNA microarray analysis. Viral suppression was more effective in GALT of PHI patients than CHI patients during HAART. Mucosal CD4+ T-cell restoration was delayed compared to peripheral blood and independent of the time of HAART initiation. Immunophenotypic analysis showed that repopulating mucosal CD4+ T cells were predominantly of a memory phenotype and expressed CD11 alpha, alpha(E)beta 7, CCR5, and CXCR4. Incomplete suppression of viral replication in GALT during HAART correlated with increased HIV-specific CD8+ T-cell responses. DNA microarray analysis revealed that genes involved in inflammation and cell activation were up regulated in patients who did not replenish mucosal CD4+ T cells efficiently, while expression of genes involved in growth and repair was increased in patients with efficient mucosal CD4+ T-cell restoration. Our findings suggest that the discordance in CD4+ T-cell restoration between GALT and peripheral blood during therapy can be attributed to the incomplete viral suppression and increased immune activation and inflammation that may prevent restoration of CD4+ T cells and the gut microenvironment.
尽管肠道相关淋巴组织(GALT)是人类免疫缺陷病毒(HIV)复制及严重CD4+ T细胞耗竭的重要早期部位,但我们对高效抗逆转录病毒治疗(HAART)期间肠道黏膜免疫系统的恢复情况了解有限。我们使用流式细胞术、实时聚合酶链反应和DNA微阵列分析,评估了原发性HIV感染(PHI)或慢性HIV感染(CHI)期间开始接受HAART治疗的患者的纵向胃肠道活检和外周血样本中病毒抑制动力学、CD4+ T细胞恢复、基因表达及HIV特异性CD8+ T细胞反应。在HAART期间,PHI患者的GALT中病毒抑制比CHI患者更有效。与外周血相比,黏膜CD4+ T细胞恢复延迟,且与开始HAART的时间无关。免疫表型分析显示,重新填充的黏膜CD4+ T细胞主要为记忆表型,并表达CD11α、α(E)β7、CCR5和CXCR4。HAART期间GALT中病毒复制的不完全抑制与HIV特异性CD8+ T细胞反应增加相关。DNA微阵列分析显示,在黏膜CD4+ T细胞未有效补充的患者中,参与炎症和细胞活化的基因上调,而在黏膜CD4+ T细胞有效恢复的患者中,参与生长和修复的基因表达增加。我们的研究结果表明,治疗期间GALT和外周血之间CD4+ T细胞恢复的不一致可能归因于病毒抑制不完全以及免疫激活和炎症增加,这可能会阻止CD4+ T细胞和肠道微环境的恢复。