Wallis R S, Vjecha M, Amir-Tahmasseb M, Okwera A, Byekwaso F, Nyole S, Kabengera S, Mugerwa R D, Ellner J J
Department of Medicine, Case Western Reserve University, Cleveland, Ohio.
J Infect Dis. 1993 Jan;167(1):43-8. doi: 10.1093/infdis/167.1.43.
Tuberculosis results in activation of T cells and macrophages that may harbor latent human immunodeficiency virus (HIV-1). Although such activation is beneficial to the host in terms of mycobacterial disease, it may be deleterious in terms of HIV-1. In Ugandan HIV-1-seropositive patients with pulmonary tuberculosis, antigen-induced blastogenesis and production of tumor necrosis factor-alpha (a cytokine that induces expression of HIV-1 in latently infected cells) were 3-10 times greater than in controls. The mean serum beta 2-microglobulin level was 5.22 mg/L in recently diagnosed patients, significantly greater than levels in HIV-negative patients with tuberculosis or asymptomatic HIV-1-seropositive subjects. beta 2-microglobulin was significantly lower in subjects who had completed at least 2 months of antituberculous therapy. These observations suggest that HIV-1-associated tuberculosis is accompanied by immune activation that may result in increased HIV expression and accelerated progression to AIDS.
结核病会导致T细胞和巨噬细胞活化,而这些细胞可能潜伏着人类免疫缺陷病毒(HIV-1)。虽然这种活化在对抗分枝杆菌疾病方面对宿主有益,但对HIV-1而言可能是有害的。在乌干达患有肺结核的HIV-1血清阳性患者中,抗原诱导的母细胞生成以及肿瘤坏死因子-α(一种在潜伏感染细胞中诱导HIV-1表达的细胞因子)的产生比对照组高3至10倍。最近诊断出的患者血清β2-微球蛋白平均水平为5.22mg/L,显著高于患结核病的HIV阴性患者或无症状HIV-1血清阳性受试者。在完成至少2个月抗结核治疗的受试者中,β2-微球蛋白水平显著降低。这些观察结果表明,与HIV-1相关的结核病伴有免疫活化,这可能导致HIV表达增加并加速发展为艾滋病。