Mycobacterium tuberculosis enhances human immunodeficiency virus-1 replication in the lung
Mycobacterium tuberculosis enhances human immunodeficiency virus-1 replication in the lung
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DOI：
10.1164/ajrccm.155.3.9117038
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发表时间：
1997-03-01
影响因子：
24.7
通讯作者：
Weiden, M
中科院分区：
文献类型：
--
作者：
Nakata, K;Rom, WN;Weiden, M
我们研究了在体内结核分枝杆菌共感染对人类免疫缺陷病毒1型（HIV-1）复制支气管肺泡灌洗（BAL）的11例HIV-1感染的肺结核和10例无肺部疾病的患者。与肺结核或无肺部疾病患者的BAL肺段相比，肺结核肺段BAL中HIV-1分支DNA（bDNA）水平和p24水平显著升高。肺结核患者的BAL病毒负荷高于血浆HIV-1，表明局部产生病毒。在3例接受连续支气管镜检查的患者中，BAL HIV-1 bDNA在结核病治疗过程中下降。肿瘤坏死因子-α（TNF-α）和HIV-1 bDNA颗粒在肺结核受累肺段中具有强相关性（r（2）= 0.9，p < 0.01）。3例肺结核患者HIV-1gp 120 V3区的推导氨基酸序列发生了与病毒表型改变相关的碱基替换。V3序列的系统发育分析表明，BAL HIV-1 RNA已从血浆中分离出来。这些数据支持肺结核增强局部HIV-1体内复制的结论。
We investigated the in vivo effect of coinfection of Mycobacterium tuberculosis on human immunodeficiency virus type 1 (HIV-1) replication using bronchoalveolar lavage (BAL) of 11 HIV-1-infected patients with pulmonary tuberculosis and 10 patients with no lung disease. Lung segments involved with pulmonary tuberculosis had significantly elevated HIV-1 branched DNA (bDNA) levels and p24 in BAL compared with lung segments uninvolved with tuberculosis or with BAL from patients with no lung disease. The BAL viral burden was higher than plasma HIV-1 in tuberculosis patients, indicating local production of virus. BAL HIV-1 bDNA declined over the course of treatment for tuberculosis in three patients who underwent serial bronchoscopies. Tumor necrosis factor-alpha (TNF-alpha) and HIV-1 bDNA particles were strongly correlated (r(2) = 0.9, p < 0.01) in lung segments involved with tuberculosis. The deduced amino acid sequence of HIV-1 gp120 V3 region from involved segments of three patients with pulmonary tuberculosis showed basic substitutions associated with altered viral phenotype. Phylogenetic analysis of V3 sequences demonstrated that BAL HIV-1 RNA had diverged from plasma. These data support the conclusion that pulmonary tuberculosis enhances local HIV-1 replication in vivo.