Immune-based therapy using gamma interferon ingaron in the treatment of HIV/AIDS patients with active pulmonary tuberculosis (PTB) not previously highly active antiretroviral therapy (HAART)

Yola, Auwal; Сологуб, Т. В.; Nechaev, Vitaly; Иванов, А. К.

doi:10.1186/1742-4690-3-s1-s38

Cited by 4 publications

(2 citation statements)

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“…A strong IFN response during the acute infection is extremely important to restrict HIV (44)(45)(46)(47)(48). In contrast, persistent chronic immune activation is associated with cellular and humoral immune dysfunction and failure to control viral replication (49,50).…”

Section: Discussionmentioning

confidence: 99%

Multiple Homozygous Variants in the STING-Encoding TMEM173 Gene in HIV Long-Term Nonprogressors

Nissen

Pedersen

Helleberg

et al. 2018

The Journal of Immunology

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Among HIV-infected individuals, long-term nonprogressor (LTNP) patients experience slow CD4 T cell decline and almost undetectable viral load for several years after primary acquisition of HIV. Type I IFN has been suggested to play a pathogenic role in HIV pathogenesis, and therefore diminished IFN responses may underlie the LTNP phenotype. In this study, we examined the presence and possible immunological role of multiple homozygous single-nucleotide polymorphisms in the stimulator of IFN genes (STING) encoding gene involved in IFN induction and T cell proliferation in HIV LTNP patients. We identified LTNPs through the Danish HIV Cohort and performed genetic analysis by Sanger sequencing, covering the R71H-G230A-R293Q (HAQ) single-nucleotide polymorphisms in This was followed by investigation of STING mRNA and protein accumulation as well as innate immune responses and proliferation following STING stimulation and infection with replication-competent HIV in human blood-derived cells. We identified G230A-R293Q/G230A-R293Q and HAQ/HAQ homozygous variants in 2 out of 11 LTNP patients. None of the 11 noncontrollers on antiretroviral treatment were homozygous for these variants. We found decreased innate immune responses to DNA and HIV as well as reduced STING-dependent inhibition of CD4 T cell proliferation, particularly in the HAQ/HAQ HIV LTNP patients, compared with the age- and gender-matched noncontrollers on antiretroviral treatment. These findings suggest that homozygous HAQ STING variants contribute to reduced inhibition of CD4 T cell proliferation and a reduced immune response toward DNA and HIV, which might result in reduced levels of constitutive IFN production. Consequently, the HAQ/HAQ genotype may contribute to the slower disease progression characteristic of LTNPs.

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Section: Discussionmentioning

confidence: 99%

Multiple Homozygous Variants in the STING-Encoding TMEM173 Gene in HIV Long-Term Nonprogressors

Nissen

Pedersen

Helleberg

et al. 2018

The Journal of Immunology

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“…Gamma interferon therapy in patients co-infected with HIV and tuberculosis receiving TB medications is safe, improves clinical outcome and enhances host defense mechanism (Yola et al, 2006). Recombinant IFN gamma-1b adjuvant therapy plus DOTS in cavitary pulmonary tuberculosis can reduce inflammatory cytokines at the site of disease, improve clearance of bacilli from the sputum, and improve constitutional symptoms (Dawson et al, 2009).…”

Section: Clinical Trials and Case Report Of Aerosolized Or Systemicalmentioning

confidence: 99%

Adjuvant Interferon Gamma in the Management of Multidrug - Resistant Tuberculosis

García-García¹,

Milanés-Virelles²,

López-Saura³

et al. 2012

Understanding Tuberculosis - Analyzing the Origin of Mycobacterium Tuberculosis Pathogenicity

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Please use Adobe Acrobat Reader to read this book chapter for free. Just open this same document with Adobe Reader. If you do not have it, you can download it here. You can freely access the chapter at the Web Viewer here. Understanding Tuberculosis-Analyzing the Origin of Mycobacterium Tuberculosis Pathogenicity 502 Please use Adobe Acrobat Reader to read this book chapter for free. Just open this same document with Adobe Reader. If you do not have it, you can download it here. You can freely access the chapter at the Web Viewer here.

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Modeling the immune rheostat of macrophages in the lung in response to infection

Day¹,

Friedman²,

Schlesinger

2009

Proc. Natl. Acad. Sci. U.S.A.

127

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In the lung, alternatively activated macrophages (AAM) form the first line of defense against microbial infection. Due to the highly regulated nature of AAM, the lung can be considered as an immunosuppressive organ for respiratory pathogens. However, as infection progresses in the lung, another population of macrophages, known as classically activated macrophages (CAM) enters; these cells are typically activated by IFN-␥. CAM are far more effective than AAM in clearing the microbial load, producing proinflammatory cytokines and antimicrobial defense mechanisms necessary to mount an adequate immune response. Here, we are concerned with determining the first time when the population of CAM becomes more dominant than the population of AAM. This proposed ''switching time'' is explored in the context of Mycobacterium tuberculosis (MTb) infection. We have developed a mathematical model that describes the interactions among cells, bacteria, and cytokines involved in the activation of both AAM and CAM. The model, based on a system of differential equations, represents a useful tool to analyze strategies for reducing the switching time, and to generate hypotheses for experimental testing.alternatively activated macrophages ͉ lung innate immunity ͉ mycobacteria tuberculosis

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Immune-based therapy using gamma interferon ingaron in the treatment of HIV/AIDS patients with active pulmonary tuberculosis (PTB) not previously highly active antiretroviral therapy (HAART)

Cited by 4 publications

References 0 publications

Multiple Homozygous Variants in the STING-Encoding TMEM173 Gene in HIV Long-Term Nonprogressors

Multiple Homozygous Variants in the STING-Encoding TMEM173 Gene in HIV Long-Term Nonprogressors

Adjuvant Interferon Gamma in the Management of Multidrug - Resistant Tuberculosis

Modeling the immune rheostat of macrophages in the lung in response to infection

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