Virological and immunological impact of tuberculosis on human immunodeficiency virus type 1 disease
Virological and immunological impact of tuberculosis on human immunodeficiency virus type 1 disease
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DOI：
10.1086/378676
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发表时间：
2003-10-15
影响因子：
6.4
通讯作者：
Toossi, Z
中科院分区：
文献类型：
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作者：
Toossi, Z
与其他与人类免疫缺陷病毒（HIV）1型相关的机会性感染不同，结核病（TB）发生在HIV-1感染的整个过程中，并且作为一种慢性感染，其对病毒活性的影响是持续的。在双重感染受试者中，活动性TB期间局部和全身HIV-1载量和异质性均增加。过去十年的研究表明，结核分枝杆菌（MTB）感染通过宿主细胞因子、趋化因子及其受体的失调支持HIV-1的复制和传播。此外，HIV-1抑制性趋化因子的浓度在TB期间和在MTB感染部位是有限的。累积起来，这些数据表明，TB提供了一个连续的细胞活化和细胞因子和趋化因子回路中的不规则性的环境，这允许病毒在原位复制和扩增。我解决了新的研究，已经确定了结核病期间HIV-1复制增强的基础，并讨论了结核病期间遏制病毒扩张的潜在免疫疗法。
Unlike other opportunistic infections associated with human immunodeficiency virus (HIV) type 1, tuberculosis ( TB) occurs throughout the course of HIV-1 infection, and, as a chronic infection, its impact on viral activity is sustained. In dually infected subjects, HIV-1 load and heterogeneity are increased both locally and systemically during active TB. Studies over the past decade have indicated that Mycobacterium tuberculosis (MTB) infection supports HIV-1 replication and dissemination through the dysregulation of host cytokines, chemokines, and their receptors. Furthermore, concentrations of HIV-1 inhibitory chemokines are limited during TB and at sites of MTB infection. Cumulatively, these data indicate that TB provides a milieu of continuous cellular activation and irregularities in cytokine and chemokine circuits that are permissive of viral replication and expansion in situ. I address new research that has identified the basis for the augmentation of HIV-1 replication during TB and discuss potential immunotherapies to contain viral expansion during TB.