| Literature DB >> 29490165 |
Hanif Esmail1,2,3, Catherine Riou1, Elsa du Bruyn1, Rachel Pei-Jen Lai4, Yolande X R Harley1, Graeme Meintjes1, Katalin A Wilkinson1,4, Robert J Wilkinson1,2,4.
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.Entities:
Keywords: HIV-1 infection; drug therapy; immune response; pathogenesis; tuberculosis
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Year: 2018 PMID: 29490165 DOI: 10.1146/annurev-immunol-042617-053420
Source DB: PubMed Journal: Annu Rev Immunol ISSN: 0732-0582 Impact factor: 28.527