Post-COVID Interstitial Lung Disease and Other Lung Sequelae

Barash, Mark; Ramalingam, Vijaya Sivalingam

doi:10.1016/j.ccm.2022.11.019

Cited by 5 publications

(3 citation statements)

References 94 publications

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“…27 However, the study by Wendisch et al identified a causal relationship between COVID-19 and idiopathic pulmonary fibrosis, 28 which was not corroborated in our study (p = 0.329). In addition, previous studies have widely confirmed that COVID-19 causes interstitial lung disease, 29,30 yet the MR analysis we used failed to confirm this finding. (STable 1)…”

Section: Discussionmentioning

confidence: 72%

Causal associations between COVID-19 and diseases of seven organs: A proteome-wide Mendelian randomization study

Shen,

Zhang,

et al. 2024

Preprint

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The coronavirus disease 2019 (COVID-19) pandemic poses an enormous threat to public health worldwide. Many retrospective studies and case reports to date have shown associations between severe COVID-19 and multi-organs. However, the research on the causal mechanisms behind this phenomenon is neither extensive nor comprehensive. We conducted a proteome-wide Mendelian randomization (MR) study using summary statistics from a genome-wide association study (GWAS) of severe COVID-19 and diseases related to seven organs: lung, spleen, liver, heart, kidney, testis, and thyroid, based on the European ancestry. We filtered the data using multi-organ proteomic data from autopsies of COVID-19 cases from previous studies. The primary analytical method used is the radial inverse variance-weighted (radial IVW) method, supplemented with the inverse variance-weighted (IVW), weighted-median (WM), MR-Egger methods. Our findings have confirmed the association between severe COVID-19 and multiple organ-related diseases, such as Hypothyroidism, strict autoimmune (HTCBSA), Thyroid disorders (TD), and Graves’ disease (GD). However, we did not find correlations between severe COVID-19 and certain organ-related diseases that have been clinically established. And we’ve also identified some proteins that are associated with organ-related disease.

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Section: Discussionmentioning

confidence: 72%

Causal associations between COVID-19 and diseases of seven organs: A proteome-wide Mendelian randomization study

Shen,

Zhang,

et al. 2024

Preprint

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“…What does seem to be common among patients with PASC are the components of fatigue, neurocognitive dysfunction, anxiety, depression, muscle pain and/or weakness, and dyspnea [ 13 ]. Other symptoms, that are either exacerbated (if preexistent before initial CoV-2 infection) or new onset, include major organ dysfunction such as lung inflammation and fibrosis [ 14 ], cardiac dysfunction such as acute myocardial infarction and myocarditis [ 15 ], hepatitis [ 16 ], kidney failure [ 17 ], new-onset diabetes mellitus [ 18 ] and other less common organ-specific manifestations [ 19 ]. Multiple reports indicate the common presence of dysautonomias which can manifest as postural orthostatic hypotension, cardiac dysrhythmias, gastrointestinal motility disorders, and others [ 20 ].…”

Section: Challenges From Pasc For Researchers and Cliniciansmentioning

confidence: 99%

The pathophysiology of postacute sequelae of COVID-19 (PASC): Possible role for persistent inflammation

Marshall

2023

Asia Pacific Allergy

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Background: As the SARS-CoV-2-induced pandemic wanes, a substantial number of patients with acute Corona Virus-induced disease (COVID-19 continue to have symptoms for a prolonged time after initial infection. These patients are said to have postacute sequelae of COVID (PASC) or “long COVID”. The underlying pathophysiology of this syndrome is poorly understood and likely quite heterogeneous. The role of persistent, possibly deviant inflammation as a major factor in comorbidity is suspected. Objective: To review data that address the relative importance of inflammation in the pathophysiology spectrum of PASC and to address how this would impact diagnosis and approach to therapy in patients identified as having such inflammatory abnormalities. Methods: A review of public databases, including PubMed, MeSH, NLM catalog, and clinical trial databases such as clinicaltrials.gov. Results: The literature supports a prominent role for various forms and types of inflammation in the pathophysiologic spectrum of PASC. Such inflammation can be persistent ant CoV-2-specific responses, new onset autoimmune responses, or a loss of normal immunoregulation resulting in widespread, sustained inflammatory pathologies that can affect both broad constitutional symptoms (such as fatigue, neurocognitive dysfunction, and anxiety/depression) and organ-specific dysfunction and/or failure. Conclusions: PASC is a significant clinical entity with similarities to and differences from other postviral syndromes. Significant research efforts are ongoing to better understand specific aberrant inflammatory pathways present in individual patients for the purpose of developing and implementing effective therapies and ultimately prophylaxis strategies to prevent the progression of COVID-19 as well as likely future viral illnesses and pandemics.

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“…Persistent complications following SARS-CoV-2 infection are well-recognized, and include persistent cough, dyspnea, hypoxemia, and interstitial lung disease [1][2][3][4][5][6][7][8][9][10] . Risk is especially high among patients who were hospitalized with severe COVID illness, and symptoms may persist for months or years after infection 2,8 .…”

Section: Introductionmentioning

confidence: 99%

Distinct Type 1 Immune Networks Underlie the Severity of Restrictive Lung Disease after COVID-19

Canderan,

Muehling,

Kadl

et al. 2024

Preprint

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The variable etiology of persistent breathlessness after COVID-19 have confounded efforts to decipher the immunopathology of lung sequelae. Here, we analyzed hundreds of cellular and molecular features in the context of discrete pulmonary phenotypes to define the systemic immune landscape of post-COVID lung disease. Cluster analysis of lung physiology measures highlighted two phenotypes of restrictive lung disease that differed by their impaired diffusion and severity of fibrosis. Machine learning revealed marked CCR5+CD95+ CD8+ T-cell perturbations in mild-to-moderate lung disease, but attenuated T-cell responses hallmarked by elevated CXCL13 in more severe disease. Distinct sets of cells, mediators, and autoantibodies distinguished each restrictive phenotype, and differed from those of patients without significant lung involvement. These differences were reflected in divergent T-cell-based type 1 networks according to severity of lung disease. Our findings, which provide an immunological basis for active lung injury versus advanced disease after COVID-19, might offer new targets for treatment.

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Post-COVID Interstitial Lung Disease and Other Lung Sequelae

Cited by 5 publications

References 94 publications

Causal associations between COVID-19 and diseases of seven organs: A proteome-wide Mendelian randomization study

Causal associations between COVID-19 and diseases of seven organs: A proteome-wide Mendelian randomization study

The pathophysiology of postacute sequelae of COVID-19 (PASC): Possible role for persistent inflammation

Distinct Type 1 Immune Networks Underlie the Severity of Restrictive Lung Disease after COVID-19

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