Pathogenesis of Human Immunodeficiency Virus-Mycobacterium tuberculosis Co-Infection

被引:23
|
作者
Wong, Kevin [1 ]
Nguyen, James [1 ]
Blair, Lillie [1 ]
Banjanin, Marina [1 ]
Grewal, Bunraj [1 ]
Bowman, Shane [1 ]
Boyd, Hailey [1 ]
Gerstner, Grant [1 ]
Cho, Hyun Jun [1 ]
Panfilov, David [1 ]
Tam, Cho Ki [1 ]
Aguilar, Delaney [1 ]
Venketaraman, Vishwanath [1 ,2 ]
机构
[1] Western Univ Hlth Sci, Coll Osteopath Med Pacific NorthWest, Lebanon, OR 97355 USA
[2] Western Univ Hlth Sci, Coll Osteopath Med Pacific, Pomona, CA 91766 USA
基金
美国国家卫生研究院;
关键词
HIV; tuberculosis; glutathione; T cell exhaustion; granuloma formation; TNF-α tumor necrosis factor; RECONSTITUTION INFLAMMATORY SYNDROME; MULTIDRUG-RESISTANT TUBERCULOSIS; TUMOR NECROSIS FACTOR; HIV-INFECTED PERSONS; T-CELL EXHAUSTION; ANTIRETROVIRAL THERAPY; GLUTATHIONE DEFICIENCY; CYTOKINE BALANCE; DENDRITIC CELLS; INDUCTION;
D O I
10.3390/jcm9113575
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Given that infection with Mycobacterium tuberculosis (Mtb) is the leading cause of death amongst individuals living with HIV, understanding the complex mechanisms by which Mtb exacerbates HIV infection may lead to improved treatment options or adjuvant therapies. While it is well-understood how HIV compromises the immune system and leaves the host vulnerable to opportunistic infections such as Mtb, less is known about the interplay of disease once active Mtb is established. This review explores how glutathione (GSH) depletion, T cell exhaustion, granuloma formation, and TNF-alpha upregulation, as a result of Mtb infection, leads to an increase in HIV disease severity. This review also examines the difficulties of treating coinfected patients and suggests further research on the clinical use of GSH supplementation.
引用
收藏
页码:1 / 23
页数:23
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