Enhanced susceptibility of blood monocytes from patients with pulmonary tuberculosis to productive infection with human immunodeficiency virus type 1.
Enhanced susceptibility of blood monocytes from patients with pulmonary tuberculosis to productive infection with human immunodeficiency virus type 1.
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肺结核患者的血单核细胞对 1 型人类免疫缺陷病毒的生产性感染的易感性增强。
DOI：
10.1084/jem.177.5.1511
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Rich,EA
中科院分区：
文献类型：
--
作者：
Toossi,Z;Sierra-Madero,JG;Blinkhorn,RA;Mettler,MA;Rich,EA
活动性肺结核患者和年龄匹配的健康纯化蛋白衍生物反应性供体的血单核细胞感染了人类免疫缺陷病毒 1 型 (HIV-1) jg。 Ft 体外评估其对 HIV-1 生产性感染的易感性。结核病患者感染细胞上清液中的 HIV-1 p24 水平（酶联免疫吸附测定）虽然存在差异，但在培养第 10-20 天时明显较高；来自患者的HIV-1感染的单核细胞上清液中p24抗原的最大水平高于对照的最大水平（P<0.05）。患者 p24 水平的最大增量也超过了对照组 (p<0.05)。使用 HIV-1 R/U5 引物对通过聚合酶链式反应测量的 HIV-1 进入和/或逆转录起始在患者和对照的受感染单核细胞中是可变的且较低，并且与 HIV-1 p24 水平不相关。通过终点稀释病毒培养物评估的感染细胞的频率对于两组来说是相似的。因此，活动性结核病患者的血液单核细胞可以产生高产的 HIV-1 感染，这似乎并不是由于 HIV 进入增强或受感染细胞频率较高所致。易感性的增强可能是由于原位暴露于结核分枝杆菌及其产物而激活单核细胞直接导致的。
Blood monocytes from patients with active pulmonary tuberculosis and age-matched healthy purified protein derivative-reactive donors were infected with human immunodeficiency virus type 1 (HIV-1) jg. Ft in vitro to assess their susceptibility to productive infection by HIV-1. HIV-1 p24 levels (enzyme-linked immunosorbent assay) in supernatants of infected cells from patients with tuberculosis, albeit variable, were significantly higher at days 10-20 of culture; the maximum levels of p24 antigen were greater in supernatants of HIV-l-infected monocytes from patients than maximum levels for controls (P< 0.05). The maximum increment in p24 levels for patients also exceeded that for controls (p< 0.05). Entry of HIV-1 and/or initiation of reverse transcription, measured by polymerase chain reaction using HIV-1 R/U5 primer pairs, was variable and low in infected monocytes from both patients and controls, and did not correlate with HIV-1 p24 levels. The frequency of infected cells as assessed by endpoint dilution viral cultures was similar for both groups. Therefore, blood monocytes from patients with active tuberculosis can develop a highly productive infection with HIV-1 that does not appear to be due to enhanced HIV entry or higher frequency of infected cells. The enhanced susceptibility may result directly from activation of monocytes by exposure to Mycobacterium tuberculosis and its products in situ.