Collins Kalonji R, Quiñones-Mateu Miguel E, Toossi Zahra, Arts Eric J
Molecular Virology Program, Case Western Reserve University, Biomedical Research Building 10th, 2109 Adelbert rd, Cleveland, OH 44106-4984, USA.
AIDS Rev. 2002 Jul-Sep;4(3):165-76.
HIV and Mycobacterium tuberculosis not only co-circulate throughout the developing world but each has contributed to prevalence and mortality caused by the other. Several reports have described how HIV-1 increases the incidence of new M. tuberculosis infections, exacerbates the severity of tuberculosis (TB), and re-activates latent M. tuberculosis. However, the converse relationship is more difficult to understand considering TB can emerge in asymptomatic individuals and as an opportunistic infection during AIDS. Development of TB in HIV infected individuals with higher CD4 cell counts (> 200/mm3) appears to increase the rate of disease progression and mortality. Higher viral loads, increased HIV-1 diversity, and changes in cytokine/chemokine levels in HIV-infected individuals with TB appear to be related to a localized immune stimulation. Specifically, increased levels of TNF alpha and MCP-1, induced by TB, may activate HIV replication in lymphocytes, monocytes, and macrophages that are resident or have migrated to M. tuberculosis infected organs (e.g. pleura or lung). The HIV-1 found in blood following this TB-mediated burst in load and diversity appear to be phylogenetically-related to HIV-1 clones that have evolved independently in the lung or pleural compartments, now infected by M. tuberculosis.
人类免疫缺陷病毒（HIV）和结核分枝杆菌不仅在整个发展中世界共同传播，而且彼此都导致了对方所引发疾病的流行率和死亡率。几份报告描述了HIV-1如何增加新的结核分枝杆菌感染的发生率、加剧结核病（TB）的严重程度以及激活潜伏的结核分枝杆菌。然而，相反的关系更难理解，因为结核病可在无症状个体中出现，并作为艾滋病期间的机会性感染出现。在CD4细胞计数较高（>200/mm³）的HIV感染者中发生结核病似乎会增加疾病进展和死亡率。结核病患者中较高的病毒载量、HIV-1多样性增加以及细胞因子/趋化因子水平的变化似乎与局部免疫刺激有关。具体而言，由结核病诱导的肿瘤坏死因子α（TNFα）和单核细胞趋化蛋白-1（MCP-1）水平升高，可能会激活驻留在或迁移到结核分枝杆菌感染器官（如胸膜或肺部）的淋巴细胞、单核细胞和巨噬细胞中的HIV复制。在这种由结核病介导的病毒载量和多样性激增后在血液中发现的HIV-1，在系统发育上似乎与在肺部或胸膜腔室中独立进化、现在被结核分枝杆菌感染的HIV-1克隆有关。
