Expanding the spectrum of HIV-associated myopathy

Gallay, Laure; Dubourg, Odile; Maisonobe, Thierry; Léonard-Louis, Sarah; Beniken, D.; Simon, Anne; Béhin, Anthony; Stojkovic, Tanya; Duyckaerts, Charles; Breton, G.; Rigolet, Aude; Fain, Olivier; Meyohas, Marie-Caroline; Leport, Catherine; Valantin, Marc‐Antoine; Vittecoq, D.; Bergmann, Jean‐François; Hanslik, Thomas; Chauveheid, Marie-Paule; Amoura, Zahir; Broucker, T. de; Eymard, B.; Beaudequin, Nausicaa; Benveniste, Olivier; Allenbach, Yves

doi:10.1136/jnnp-2018-319419

Cited by 7 publications

(4 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The skeletal muscles can be subject to damage during all stages of infection with human immunodeficiency virus (HIV). Broadly, damage to skeletal muscle in association with HIV can be attributed to inflammatory mechanisms or toxicity of anti-retroviral therapy [ 42 ]. With respect to the former, the virus itself may provoke ephemeral myalgia during seroconversion, while a pro-inflammatory state results from specific alterations of the immune architecture during the disease that may occur even despite clinically effective treatment.…”

Section: Ibm and The Human Immunodeficiency Virusmentioning

confidence: 99%

“…‘HIV myopathy’ has been used as an umbrella term including both toxic (cART-related) and inflammatory myopathies in the context of HIV infection. In a follow up study on HIV myopathy, skeletal muscle biopsies from 46 HIV-positive patients were categorized into five subgroups according to European Neuromuscular Center (ENMC) criteria [ 42 ]. Here, IBM accounted for 3 patients, while 18 were classified as PM, 1 as IMNM and 12 as non-specific myositis.…”

Section: Ibm and The Human Immunodeficiency Virusmentioning

confidence: 99%

“…Here, IBM accounted for 3 patients, while 18 were classified as PM, 1 as IMNM and 12 as non-specific myositis. In addition, 12 patients displayed isolated mitochondrial abnormalities with COX-negative fibers and without rimmed vacuoles or inflammation [ 42 ]. Of note, virus-specific antigens were not detected and only a minor subset of T cells were found to be clonally expanded [ 16 ].…”

Section: Ibm and The Human Immunodeficiency Virusmentioning

confidence: 99%

See 2 more Smart Citations

Inclusion body myositis and associated diseases: an argument for shared immune pathologies

Nelke

Kleefeld

Preuße

et al. 2022

acta neuropathol commun

View full text Add to dashboard Cite

Inclusion body myositis (IBM) is the most prevalent idiopathic inflammatory myopathy (IIM) affecting older adults. The pathogenic hallmark of IBM is chronic inflammation of skeletal muscle. At present, we do not classify IBM into different sub-entities, with the exception perhaps being the presence or absence of the anti-cN-1A-antibody. In contrast to other IIM, IBM is characterized by a chronic and progressive disease course. Here, we discuss the pathophysiological framework of IBM and highlight the seemingly prototypical situations where IBM occurs in the context of other diseases. In this context, understanding common immune pathways might provide insight into the pathogenesis of IBM. Indeed, IBM is associated with a distinct set of conditions, such as human immunodeficiency virus (HIV) or hepatitis C—two conditions associated with premature immune cell exhaustion. Further, the pathomorphology of IBM is reminiscent of other muscle diseases, notably HIV-associated myositis or granulomatous myositis. Distinct immune pathways are likely to drive these commonalities and senescence of the CD8+ T cell compartment is discussed as a possible mechanism of pathogenesis. Future effort directed at understanding the co-occurrence of IBM and associated diseases could prove valuable to better understand the enigmatic IBM pathophysiology.

show abstract

Section: Ibm and The Human Immunodeficiency Virusmentioning

confidence: 99%

Section: Ibm and The Human Immunodeficiency Virusmentioning

confidence: 99%

Section: Ibm and The Human Immunodeficiency Virusmentioning

confidence: 99%

See 1 more Smart Citation

Inclusion body myositis and associated diseases: an argument for shared immune pathologies

Nelke

Kleefeld

Preuße

et al. 2022

acta neuropathol commun

View full text Add to dashboard Cite

show abstract

“…HIV-associated myositis has been described as a complication of HIV/AIDS since the beginning of the HIV/AIDS pandemic [ 1 ]. Different subtypes of myositis can occur in the context of HIV infection and may be classified into the following groups: isolated mitochondrial abnormalities (IMA), polymyositis (PM), inclusion body myositis (IBM), Immune-mediated necrotizing myopathy (IMNM) and non-specific myositis [ 2 ]. HIV-infected patients who develop IBM have been shown to differ from sporadic IBM (sIBM) patients in terms of earlier onset of illness and, in some cases, better response to immunomodulatory treatment [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

Morphological and molecular comparison of HIV-associated and sporadic inclusion body myositis

Vogt,

Kleefeld,

Preusse

et al. 2023

J Neurol

View full text Add to dashboard Cite

Objective The molecular characteristics of sporadic inclusion body myositis (sIBM) have been intensively studied, and specific patterns on the cellular, protein and RNA level have emerged. However, these characteristics have not been studied in the context of HIV-associated IBM (HIV-IBM). In this study, we compared clinical, histopathological, and transcriptomic patterns of sIBM and HIV-IBM. Methods In this cross-sectional study, we compared patients with HIV-IBM and sIBM based on clinical and morphological features as well as gene expression levels of specific T-cell markers in skeletal muscle biopsy samples. Non-disease individuals served as controls (NDC). Cell counts for immunohistochemistry and gene expression profiles for quantitative PCR were used as primary outcomes. Results 14 muscle biopsy samples (7 HIV-IBM, 7 sIBM) of patients and 6 biopsy samples from NDC were included. Clinically, HIV-IBM patients showed a significantly lower age of onset and a shorter period between symptom onset and muscle biopsy. Histomorphologically, HIV-IBM patients showed no KLRG1+ or CD57+ cells, while the number of PD1+ cells did not differ significantly between the two groups. All markers were shown to be significantly upregulated at gene expression level with no significant difference between the IBM subgroups. Conclusion Despite HIV-IBM and sIBM sharing important clinical, histopathological, and transcriptomic signatures, the presence of KLRG1+ cells discriminated sIBM from HIV-IBM. This may be explained by longer disease duration and subsequent T-cell stimulation in sIBM. Thus, the presence of TEMRA cells is characteristic for sIBM, but not a prerequisite for the development of IBM in HIV+ patients.

show abstract

Treatment and Management of Infectious, Granulomatous, and Toxic Neuromuscular Disorders

Luciano¹,

Caraballo-Cartagena²

2022

Neuromuscular Disorders

View full text Add to dashboard Cite

Expanding the spectrum of HIV-associated myopathy

Cited by 7 publications

References 5 publications

Inclusion body myositis and associated diseases: an argument for shared immune pathologies

Inclusion body myositis and associated diseases: an argument for shared immune pathologies

Morphological and molecular comparison of HIV-associated and sporadic inclusion body myositis

Treatment and Management of Infectious, Granulomatous, and Toxic Neuromuscular Disorders

Contact Info

Product

Resources

About