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

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

Author information

1
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: robert.wilkinson@crick.ac.uk.
2
Department of Medicine, Imperial College London, London W2 1PG, United Kingdom.
3
Radcliffe Department of Medicine, University of Oxford, Oxford OX3 9DU, United Kingdom.
4
The Francis Crick Institute, London NW1 2AT, United Kingdom.

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.

KEYWORDS:

HIV-1 infection; drug therapy; immune response; pathogenesis; tuberculosis

[Indexed for MEDLINE]

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