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HIV-1 共感染人群对结核分枝杆菌的免疫反应。

The Immune Response to Mycobacterium tuberculosis in HIV-1-Coinfected Persons.

机构信息

Wellcome Centre for Infectious Diseases Research in Africa, Institute of Infectious Disease and Molecular Medicine, and Department of Medicine, University of Cape Town, Cape Town 7925, Republic of South Africa; email:

Department of Medicine, Imperial College London, London W2 1PG, United Kingdom.

出版信息

Annu Rev Immunol. 2018 Apr 26;36:603-638. doi: 10.1146/annurev-immunol-042617-053420. Epub 2018 Feb 28.

DOI:10.1146/annurev-immunol-042617-053420
PMID:29490165
Abstract

Globally, about 36.7 million people were living with HIV infection at the end of 2015. The most frequent infection co-occurring with HIV-1 is Mycobacterium tuberculosis-374,000 deaths per annum are attributable to HIV-tuberculosis, 75% of those occurring in Africa. HIV-1 infection increases the risk of tuberculosis by a factor of up to 26 and alters its clinical presentation, complicates diagnosis and treatment, and worsens outcome. Although HIV-1-induced depletion of CD4 T cells underlies all these effects, more widespread immune deficits also contribute to susceptibility and pathogenesis. These defects present a challenge to understand and ameliorate, but also an opportunity to learn and optimize mechanisms that normally protect people against tuberculosis. The most effective means to prevent and ameliorate tuberculosis in HIV-1-infected people is antiretroviral therapy, but this may be complicated by pathological immune deterioration that in turn requires more effective host-directed anti-inflammatory therapies to be derived.

摘要

截至 2015 年底,全球约有 3670 万人感染了艾滋病毒。与 HIV-1 最常同时发生的感染是结核分枝杆菌,每年有 37.4 万人死于艾滋病毒-结核病,其中 75%发生在非洲。HIV-1 感染使结核病的风险增加了多达 26 倍,并改变了其临床表现,使诊断和治疗复杂化,使预后恶化。虽然 HIV-1 诱导的 CD4 T 细胞耗竭是所有这些影响的基础,但更广泛的免疫缺陷也导致了易感性和发病机制。这些缺陷对理解和改善构成了挑战,但也为学习和优化正常保护人们免受结核病的机制提供了机会。预防和改善 HIV-1 感染者结核病的最有效方法是抗逆转录病毒治疗,但这可能因病理性免疫恶化而变得复杂,反过来又需要开发更有效的宿主定向抗炎治疗。

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