scholarly journals Analysis of Antimicrobial Activity of Monocytic Myeloid-Derived Suppressor Cells in Infection with Mycobacterium tuberculosis and Human Immunodeficiency Virus

2020 ◽  
pp. 115-127
Author(s):  
Ankita Garg
Keyword(s):  
Human Immunodeficiency Virus ◽  
Antimicrobial Activity ◽  
Mycobacterium Tuberculosis ◽  
Suppressor Cells ◽  
Myeloid Derived Suppressor Cells ◽  
Immunodeficiency Virus

scholarly journals Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection

Open Biology ◽  
2021 ◽  
Vol 11 (11) ◽  
Author(s):  
Mahmoud Mohammad Yaseen ◽  
Nizar Mohammad Abuharfeil ◽  
Homa Darmani
Keyword(s):  
Human Immunodeficiency Virus ◽  
Virus Infection ◽  
Hiv Infection ◽  
Immune Activation ◽  
Suppressor Cells ◽  
Myeloid Derived Suppressor Cells ◽  
Chronic Immune Activation ◽  
Immune Suppressor Cells ◽  
Immunodeficiency Virus ◽  
Immune Suppressor

There are several mechanisms by which human immunodeficiency virus (HIV) can mediate immune dysfunction and exhaustion during the course of infection. Chronic immune activation, after HIV infection, seems to be a key driving force of such unwanted consequences, which in turn worsens the pathological status. In such cases, the immune system is programmed to initiate responses that counteract unwanted immune activation, for example through the expansion of myeloid-derived suppressor cells (MDSCs). Although the expansion of immune suppressor cells in the setting of systemic chronic immune activation, in theory, is expected to contain immune activation, HIV infection is still associated with a remarkably high level of biomarkers of immune activation. Paradoxically, the expansion of immune suppressor cells during HIV infection can suppress potent anti-viral immune responses, which in turn contribute to viral persistence and disease progression. This indicates that HIV hijacks not only immune activation but also the immune regulatory responses to its advantage. In this work, we aim to pave the way to comprehend how such unwanted expansion of MDSCs could participate in the pathology of acute/primary and chronic HIV infection in humans, as well as simian immunodeficiency virus infection in rhesus macaques, according to the available literature.

scholarly journals Monocytic-Myeloid Derived Suppressor Cells of HIV-Infected Individuals With Viral Suppression Exhibit Suppressed Innate Immunity to Mycobacterium tuberculosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Priyanka Namdev ◽  
Shiv Patel ◽  
Brandi Sparling ◽  
Ankita Garg
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Viral Suppression ◽  
Suppressor Cells ◽  
Innate Immune ◽  
Virologic Suppression ◽  
Myeloid Derived Suppressor Cells ◽  
Toll Like Receptor ◽  
Intracellular Replication ◽  
Hla Dr ◽  
Immunodeficiency Virus

Tuberculosis can occur during any stage of Human Immunodeficiency virus 1 (HIV) -infection including times when CD4+ T cell numbers have reconstituted and viral replication suppressed. We have previously shown that CD11b+CD33+CD14+HLA-DR-/lo monocytic myeloid-derived suppressor cells (MDSC) persist in HIV-infected individuals on combined anti-retroviral therapy (cART) and with virologic suppression. The response of MDSC to Mycobacterium tuberculosis (Mtb) is not known. In this study, we compared the anti-mycobacterial activity of MDSC isolated from HIV –infected individuals on cART with virologic suppression (HIV MDSC) and HIV-uninfected healthy controls (HIV (-) MDSC). Compared to HIV (-) MDSC, HIV MDSC produced significantly less quantities of anti-mycobacterial cytokines IL-12p70 and TNFα, and reactive oxygen species when cultured with infectious Mtb or Mtb antigens. Furthermore, HIV MDSC showed changes in the Toll-like receptor and IL-27 signaling, including reduced expression of MyD88 and higher levels of IL-27. Neutralizing IL-27 and overexpression of MyD88 synergistically controlled intracellular replication of Mtb in HIV MDSC. These results demonstrate that MDSC in fully suppressed HIV-infected individuals are permissive to Mtb and exhibit downregulated anti-mycobacterial innate immune activity through mechanisms involving IL-27 and TLR signaling. Our findings suggest MDSC as novel mediators of tuberculosis in HIV-Mtb co-infected individuals with virologic suppression.

scholarly journals A Randomized Controlled Trial of Isoniazid to Prevent Mycobacterium tuberculosis Infection in Kenyan Human Immunodeficiency Virus–Exposed Uninfected Infants

2020 ◽  
Author(s):  
Sylvia M LaCourse ◽  
Barbra A Richardson ◽  
John Kinuthia ◽  
A J Warr ◽  
Elizabeth Maleche-Obimbo ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Mycobacterium Tuberculosis ◽  
High Risk ◽  
Adverse Events ◽  
Controlled Trial ◽  
Preventive Therapy ◽  
Infection Prevalence ◽  
Mycobacterium Tuberculosis Infection ◽  
Immunodeficiency Virus ◽  
Exposed Uninfected

Abstract Background Human immunodeficiency virus (HIV)–exposed uninfected (HEU) infants in endemic settings are at high risk of tuberculosis (TB). For infants, progression from primary Mycobacterium tuberculosis (Mtb) infection to TB disease can be rapid. We assessed whether isoniazid (INH) prevents primary Mtb infection. Methods We conducted a randomized nonblinded controlled trial enrolling HEU infants 6 weeks of age without known TB exposure in Kenya. Participants were randomized (1:1) to 12 months of daily INH (10 mg/kg) vs no INH. Primary endpoint was Mtb infection at end of 12 months, assessed by interferon-γ release assay (QuantiFERON-TB Gold Plus) and/or tuberculin skin test (TST, added 6 months after first participant exit). Results Between 15 August 2016 and 6 June 2018, 416 infants were screened, with 300 (72%) randomized to INH or no INH (150 per arm); 2 were excluded due to HIV infection. Among 298 randomized HEU infants, 12-month retention was 96.3% (287/298), and 88.9% (265/298) had primary outcome data. Mtb infection prevalence at 12-month follow-up was 10.6% (28/265); 7.6% (10/132) in the INH arm and 13.5% (18/133) in the no INH arm (7.0 vs 13.4 per 100 person-years; hazard ratio, 0.53 [95% confidence interval {CI}, .24–1.14]; P = .11]), and driven primarily by TST positivity (8.6% [8/93] in INH and 18.1% [17/94] in no INH; relative risk, 0.48 [95% CI, .22–1.05]; P = .07). Frequency of severe adverse events was similar between arms (INH, 14.0% [21/150] vs no INH, 10.7% [16/150]; P = .38), with no INH-related adverse events. Conclusions Further studies evaluating TB preventive therapy to prevent or delay primary Mtb infection in HEU and other high-risk infants are warranted. Clinical Trials Registration NCT02613169.

Multidrug Resistant Mycobacterium tuberculosis in Patients with Human Immunodeficiency Virus Infection

CHEST Journal ◽  
1992 ◽  
Vol 102 (3) ◽  
pp. 797-801 ◽  
Author(s):  
Christopher P. Busillo ◽  
Klaus-Dieter Lessnou ◽  
Veraaf Sanjana ◽  
Sarantos Soumakis ◽  
Morton Davidson ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Mycobacterium Tuberculosis ◽  
Virus Infection ◽  
Human Immunodeficiency Virus Infection ◽  
Multidrug Resistant ◽  
Immunodeficiency Virus

scholarly journals Gr1intCD11b+ Myeloid-Derived Suppressor Cells in Mycobacterium tuberculosis Infection

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e80669 ◽  
Author(s):  
Andrés Obregón-Henao ◽  
Marcela Henao-Tamayo ◽  
Ian M. Orme ◽  
Diane J. Ordway
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Suppressor Cells ◽  
Tuberculosis Infection ◽  
Myeloid Derived Suppressor Cells ◽  
Mycobacterium Tuberculosis Infection
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