The
            <i>Mtb</i>
            -HIV Syndemic Interaction: Why Treating
            <i>M. tuberculosis</i>
            Infection May Be Crucial for HIV-1 Eradication

Waters, Robyn; Ndengane, Mthawelanga; Abrahams, Melissa-Rose; Diedrich, Collin R.; Wilkinson, Robert J.; Coussens, Anna K.

doi:10.2217/fvl-2019-0069

Cited by 31 publications

(31 citation statements)

References 196 publications

(237 reference statements)

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“…8 Likewise, alteration of glutathione and tumor necrosis factor, T-cell exhaustion and immune consumption as a result of Mycobacterium tuberculosis infection may lead to severe HIV disease. 9,10 This entails the importance of a correct pathologic diagnosis of Mycobacterium tuberculosis regardless of their various atypical nongranulomatous histopathologic manifestations for the appropriate clinical management of HIV-infected patients.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, Mycobacterium tuberculosis/HIV-coinfected patients tend to develop poorly formed or absent granulomas, debris necrosis, numerous neutrophils, suppurative abscess formation, diffuse foamy histiocytes and pseudotumor spindle histiocytoid cell proliferations. [8][9][10] The impaired immune response due to HIV-infection alters the typical hypersensitivity type-IV anti-tuberculosis response by modulating T-cell immunity and tumor necrosis factor production. 8 Likewise, alteration of glutathione and tumor necrosis factor, T-cell exhaustion and immune consumption as a result of Mycobacterium tuberculosis infection may lead to severe HIV disease.…”

Section: Discussionmentioning

confidence: 99%

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Unusual Presentations of Mycobacterium Tuberculosis in HIV-Positive Patients: A Case Series

AbdullGaffar

Abdelkareem

2022

Int J Surg Pathol

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Necrotizing and non-necrotizing epithelioid granulomatous chronic inflammation is the usual recognizable histopathologic presentation of mycobacterial infections. In immunosuppressed patients, atypical histomorphologic patterns may occur. Rare and diagnostically challenging manifestations of nontubercular mycobacterial infections in transplant and Human Immunodeficiency Virus (HIV)-infected patients include mycobacterial spindle cell pseudotumor and suppurative lesions. Lesions composed of nodular spindle cell proliferation mimicking inflammatory, histiocytoid and spindle cell tumors, and similarly suppurative lesions simulating abscesses have been mostly reported in association with nontuberculous mycobacterial infections mainly in nodal and various extranodal sites. Similar lesions related to Mycobacterium tuberculosis that involve serosal membranes are unusual and diagnostically challenging. Our aim is to report mycobacterial spindle cell pseudotumor-associated pericarditis, suppurative abscess-forming pleuritis, and cholesterol pleuritis due to tuberculosis in three HIV-infected young adult males. Initially, we confused the mycobacterial spindle cell pseudotumor for Kaposi sarcoma, the suppurative pleuritis for bacterial and fungal empyema, and the cholesterol pleuritis with rheumatoid arthritis. A prior knowledge of the immune status of our patients helped us confirm our final correct diagnosis of mycobacterial infection by performing Ziehl-Neelsen special stain. Polymerase chain reaction detected Mycobacterium tuberculosis in respiratory samples. Utilization of acid-fast special stains in all HIV-patients regardless of the histopathologic appearances, and the application of an appropriate panel of immunomarkers should help pathologists reach the correct diagnosis and avoid pitfalls. Without prior clinical knowledge, pathologists should raise this possibility in young patients with such unusual manifestations, because correct pathologic recognition is clinically important for the appropriate management of these vulnerable patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Unusual Presentations of Mycobacterium Tuberculosis in HIV-Positive Patients: A Case Series

AbdullGaffar

Abdelkareem

2022

Int J Surg Pathol

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“…Furthermore, it is well established that HIV induces changes in the gut microbiota composition ( Vujkovic-Cvijin and Somsouk, 2019 ). How these processes are affected by Mtb during HIV/TB co-infection are not yet understood ( Waters et al, 2020 ), although it is known that patients with TB also have an altered gut microbiota composition ( Winglee et al, 2014 ; Luo et al, 2017 ; Hu et al, 2019 ).…”

Section: Human Immunodeficiency Virus/tuberculosis Co-infection: What Do We Know and What Are The Current Gaps?mentioning

confidence: 99%

Metabolomics as a Tool to Investigate HIV/TB Co-Infection

Liebenberg

Luies

Williams

2021

Front. Mol. Biosci.

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The HIV/AIDS (human immunodeficiency virus/acquired immunodeficiency syndrome) and tuberculosis (TB) pandemics are perpetuated by a significant global burden of HIV/TB co-infection. The synergy between HIV and Mycobacterium tuberculosis (Mtb) during co-infection of a host is well established. While this synergy is known to be driven by immunological deterioration, the metabolic mechanisms thereof remain poorly understood. Metabolomics has been applied to study various aspects of HIV and Mtb infection separately, yielding insights into infection- and treatment-induced metabolic adaptations experienced by the host. Despite the contributions that metabolomics has made to the field, this approach has not yet been systematically applied to characterize the HIV/TB co-infected state. Considering that limited HIV/TB co-infection metabolomics studies have been published to date, this review briefly summarizes what is known regarding the HIV/TB co-infection synergism from a conventional and metabolomics perspective. It then explores metabolomics as a tool for the improved characterization of HIV/TB co-infection in the context of previously published human-related HIV infection and TB investigations, respectively as well as for addressing the gaps in existing knowledge based on the similarities and deviating trends reported in these HIV infection and TB studies.

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“…Although these inflammatory cells would ordinarily excel at pathogen killing, the intracellular effects of HIV and Mtb render the macrophages less effective and, as a result, permit ongoing pathogen growth [60]. At the same time, there is ample evidence that Mtb infection of alveolar macrophages creates a permissive environment for HIV infection and replication, through a variety of mechanisms including increased surface expression of the HIV receptors CCR5 and CXCR4, increased HIV transcription and replication, and induction of nanotubes that promote cell-to-cell HIV viral spread between macrophages [61][62][63][64]. Taken together, this synergy between Mtb-and HIV-mediated impacts on macrophages enables intracellular growth and survival of both pathogens and, more broadly, fuels the global syndemic of coinfection.…”

Section: Alveolar Macrophage Phenotypes In Mtb Infectionmentioning

confidence: 99%

HIV and the tuberculosis “set point”: how HIV impairs alveolar macrophage responses to tuberculosis and sets the stage for progressive disease

Auld

Staitieh

2020

Retrovirology

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As HIV has fueled a global resurgence of tuberculosis over the last several decades, there is a growing awareness that HIV-mediated impairments in both innate and adaptive immunity contribute to the heightened risk of tuberculosis in people with HIV. Since early immune responses to Mycobacterium tuberculosis (Mtb) set the stage for subsequent control or progression to active tuberculosis disease, early host–pathogen interactions following Mtb infection can be thought of as establishing a mycobacterial “set point,” which we define as the mycobacterial burden at the point of adaptive immune activation. This early immune response is impaired in the context of HIV coinfection, allowing for a higher mycobacterial set point and greater likelihood of progression to active disease with greater bacterial burden. Alveolar macrophages, as the first cells to encounter Mtb in the lungs, play a critical role in containing Mtb growth and establishing the mycobacterial set point. However, a number of key macrophage functions, ranging from pathogen recognition and uptake to phagocytosis and microbial killing, are blunted in HIV coinfection. To date, research evaluating the effects of HIV on the alveolar macrophage response to Mtb has been relatively limited, particularly with regard to the critical early events that help to dictate the mycobacterial set point. A greater understanding of alveolar macrophage functions impacted by HIV coinfection will improve our understanding of protective immunity to Mtb and may reveal novel pathways amenable to intervention to improve both early immune control of Mtb and clinical outcomes for the millions of people worldwide infected with HIV.

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The Mtb -HIV Syndemic Interaction: Why Treating M. tuberculosis Infection May Be Crucial for HIV-1 Eradication

Cited by 31 publications

References 196 publications

Unusual Presentations of Mycobacterium Tuberculosis in HIV-Positive Patients: A Case Series

Unusual Presentations of Mycobacterium Tuberculosis in HIV-Positive Patients: A Case Series

Metabolomics as a Tool to Investigate HIV/TB Co-Infection

HIV and the tuberculosis “set point”: how HIV impairs alveolar macrophage responses to tuberculosis and sets the stage for progressive disease

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