Chapter 12 : The Immune Interaction between HIV-1 Infection and

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HIV-1-infected people are approximately 26 times more likely to develop tuberculosis (TB) than HIV-1-uninfected people ( ). This increased risk of developing TB is apparent early after HIV-1 seroconversion: a large study of South African miners found that TB incidence doubled within the first year of HIV-1 infection ( ). Of the 9.6 million reported TB cases in 2014, 1.2 million were coinfected with HIV-1, with 74% of reported HIV-1-infected TB cases being from Africa ( ). The HIV-1 burden in sub-Saharan Africa is particularly high, where 25.8 million people were living with HIV in 2014 and only 41% had access to antiretroviral therapy (ART) ( ). The relatively low ART access may arise in part from a lack of eligibility as determined by local guidelines. It is hoped that more people living with HIV might access ART as a result of the 2015 World Health Organization (WHO) recommendation that ART be initiated for everyone living with HIV at any CD4 cell count ( ). ART reduces TB risk among HIV-1-infected people by 54 to 90% and halves the TB recurrence rate ( ). Despite this risk reduction, HIV-1-infected people established on ART in high TB burden settings remain at higher risk than HIV-1-uninfected people, even in higher CD4 strata ( ).

Citation: du Bruyn E, Wilkinson R. 2017. The Immune Interaction between HIV-1 Infection and , p 239-268. In Jacobs, Jr. W, McShane H, Mizrahi V, Orme I (ed), Tuberculosis and the Tubercle Bacillus, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.TBTB2-0012-2016
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Figure 1

Spectrum of disease in HIV-TB coinfection. The axis represents stages of tuberculosis, from infection through to active disease, while the axis represents stages of HIV-1 infection. bacterial burden and CD4 count are shown in blue along the respective axes. The spectrum of latent TB is represented as follows: infection eliminated without priming antigen-specific T cells; infection eliminated in association with T-cell priming; infection contained with some bacteria persisting in a nonreplicating form; bacterial replication maintained at the subclinical level by the immune system. Clinical disease (pulmonary and extrapulmonary tuberculosis) occurs in a subset of individuals who are latently infected or who develop primary tuberculosis directly following infection or reinfection. The annual risk is represented as follows: HIV-1-uninfected: about 10% lifetime risk or about 1% per annum (p/a); shortly after HIV-1 infection and prior to substantial CD4 T-cell depletion, the risk of active tuberculosis increases; during the early stages of HIV-1 infection, this risk rises to approximately 10% p/a; in late-stage HIV-1 infection, the risk of active tuberculosis increases to 30% p/a. The effects of HIV-1 on tuberculosis and of tuberculosis on HIV-1 disease are shown by the red arrows. Reproduced from ( ) with permission of the publisher.

Citation: du Bruyn E, Wilkinson R. 2017. The Immune Interaction between HIV-1 Infection and , p 239-268. In Jacobs, Jr. W, McShane H, Mizrahi V, Orme I (ed), Tuberculosis and the Tubercle Bacillus, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.TBTB2-0012-2016
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Figure 2

A model of innate receptor signaling in mediating TB-IRIS pathogenesis as proposed by Lai et al. Microarray profiling revealed that TLR signaling and inflammasome activation are critical in mediating TB-IRIS pathogenesis. The proposed model begins with antigen recognition by surface-expressing TLRs, which triggers the downstream signaling cascade with adaptor molecules such as MyD88 and IRAK4 to activate IRF7, thereby triggering the production of type I IFN. Paracrine signaling of type I IFN to IFNAR recruits and phosphorylates STAT1/2 dimers, leading to further recruitment of IRF9 and the formation of ISGF3, thereby inducing pro-caspase-11 (caspase-4/5 in human) and AIM-2 inflammasome (caspase-1). Caspase-11 cleaves IL-1α into its mature form and can lead to pyroptosis. The noncanonical inflammasome (caspase-11) can also activate the canonical inflammasome (caspase-1), which cleaves IL-1β and IL-18 into their mature form. Alternatively, TLR signaling via MyD88 can also activate NF-κB via the TAK1/IKK complex. Activation of NF-κB triggers the production of an array of cytokines, including TNF-α, IL-6, and IL-12. In addition, NF-κB also activates NLRP1/3 inflammasomes and subsequently leads to the production of IL-1β and IL-18. Reproduced from ( ) with permission of the publisher.

Citation: du Bruyn E, Wilkinson R. 2017. The Immune Interaction between HIV-1 Infection and , p 239-268. In Jacobs, Jr. W, McShane H, Mizrahi V, Orme I (ed), Tuberculosis and the Tubercle Bacillus, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.TBTB2-0012-2016
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