Pulmonary Sequelae at 4 Months After COVID-19 Infection: A Single-Centre Experience of a COVID Follow-Up Service

Robey, Rebecca; Kemp, Katie; Hayton, Philip; Mudawi, Dalia; Wang, Ran; Greaves, Melanie; Yioe, Veronica; Ortega, Pilar Rivera; Avram, Cristina; Chaudhuri, Nazia

doi:10.1007/s12325-021-01833-4

Cited by 26 publications

(29 citation statements)

References 36 publications

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“…1, S1, S2 ). Micro-CT detected heterogeneous subpleural opacities and fibrosis in surviving mice, similar to human studies ( 70 ). While most of acute cytokine production returned to normal levels by 30 dpi, DSP and RNA-ISH data revealed focally prolonged upregulation of cytokine signaling, including TGF-β, in sub-pleural fibrotic regions.…”

Section: Discussionsupporting

confidence: 83%

A model of persistent post SARS-CoV-2 induced lung disease for target identification and testing of therapeutic strategies

Dinnon

Leist

Okuda

et al. 2022

Preprint

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COVID-19 survivors develop post-acute sequelae of SARS-CoV-2 (PASC), but the mechanistic basis of PASC-associated lung abnormalities suffers from a lack of longitudinal samples. Mouse-adapted SARS-CoV-2 MA10 produces an acute respiratory distress syndrome (ARDS) in mice similar to humans. To investigate PASC pathogenesis, studies of MA10-infected mice were extended from acute disease through clinical recovery. At 15-120 days post-virus clearance, histologic evaluation identified subpleural lesions containing collagen, proliferative fibroblasts, and chronic inflammation with tertiary lymphoid structures. Longitudinal spatial transcriptional profiling identified global reparative and fibrotic pathways dysregulated in diseased regions, similar to human COVID-19. Populations of alveolar intermediate cells, coupled with focal upregulation of pro-fibrotic markers, were identified in persistently diseased regions. Early intervention with antiviral EIDD-2801 reduced chronic disease, and early anti-fibrotic agent (nintedanib) intervention modified early disease severity. This murine model provides opportunities to identify pathways associated with persistent SARS-CoV-2 pulmonary disease and test countermeasures to ameliorate PASC.

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Section: Discussionsupporting

confidence: 83%

A model of persistent post SARS-CoV-2 induced lung disease for target identification and testing of therapeutic strategies

Dinnon

Leist

Okuda

et al. 2022

Preprint

View full text Add to dashboard Cite

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“…Other studies have also found that survivors of more severe COVID‐19 were more likely to develop lung fibrosis and other pulmonary radiological abnormalities, as well as impaired lung function, up to 6‐ to 7‐month post‐discharge. A few of these studies also reported that long‐term pulmonary fibrosis was associated with comorbidities, male sex and older age 34–41 . Details of these studies are summarised in Table 1B.…”

Section: Resultsmentioning

confidence: 99%

“…A few of these studies also reported that long-term pulmonary fibrosis was associated with comorbidities, male sex and older age. [34][35][36][37][38][39][40][41] Details of these studies are summarised in Table 1B. Therefore, in contrast to NSC-MOS, the PFS subtype of PCS is dependent on the initial severity of acute COVID-19.…”

Section: Pulmonary Fibrosis Sequelae (Pfs)mentioning

confidence: 99%

Proposed subtypes of post‐COVID‐19 syndrome (or long‐COVID) and their respective potential therapies

Yong

Liu

2021

Reviews in Medical Virology

116

113

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The effects of coronavirus disease 2019 (COVID-19), a highly transmissible infectious respiratory disease that has initiated an ongoing pandemic since early 2020, do not always end in the acute phase. Depending on the study referred, about 10%-30% (or more) of COVID-19 survivors may develop long-COVID or post-COVID-19 syndrome (PCS), characterised by persistent symptoms (most commonly fatigue, dyspnoea, and cognitive impairments) lasting for 3 months or more after acute COVID-19. While the pathophysiological mechanisms of PCS have been extensively described elsewhere, the subtypes of PCS have not. Owing to its highly multifaceted nature, this review proposes and characterises six subtypes of PCS based on the existing literature. The subtypes are non-severe COVID-19 multi-organ sequelae (NSC-MOS), pulmonary fibrosis sequelae (PFS), myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS), postural orthostatic tachycardia syndrome (POTS), post-intensive care syndrome (PICS) and medical or clinical sequelae (MCS).Original studies supporting each of these subtypes are documented in this review, as well as their respective symptoms and potential interventions. Ultimately, the subtyping proposed herein aims to provide better clarity on the current understanding of PCS.

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“…Although PASC encompasses non-respiratory sequelae, including cardiovascular and neurologic disease ( 61 ), pulmonary manifestations are especially common, including CAP and PF ( 62 , 63 ). CT scans reveal chronic COVID-19 pulmonary findings as evidenced by ground glass opacities (44%) and fibrosis (21%) after acute COVID-19 infection ( 64 ) and fibrotic-like changes (35%) 6 months after severe human COVID-19 pneumonia ( 65 ). Pathology studies of COVID-19 lungs obtained at autopsy reveal similar late findings, such as CAP and PF ( 53 , 66 , 67 ).…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 infection produces chronic pulmonary epithelial and immune cell dysfunction with fibrosis in mice

et al. 2022

View full text Add to dashboard Cite

A subset of individuals who recover from coronavirus disease 2019 (COVID-19) develop post-acute sequelae of SARS-CoV-2 (PASC), but the mechanistic basis of PASC-associated lung abnormalities suffers from a lack of longitudinal tissue samples. The mouse-adapted severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strain MA10 produces an acute respiratory distress syndrome (ARDS) in mice similar to humans. To investigate PASC pathogenesis, studies of MA10-infected mice were extended from acute to clinical recovery phases. At 15 to 120 days post-virus clearance, pulmonary histologic findings included subpleural lesions composed of collagen, proliferative fibroblasts, and chronic inflammation, including tertiary lymphoid structures. Longitudinal spatial transcriptional profiling identified global reparative and fibrotic pathways dysregulated in diseased regions, similar to human COVID-19. Populations of alveolar intermediate cells, coupled with focal up-regulation of pro-fibrotic markers, were identified in persistently diseased regions. Early intervention with antiviral EIDD-2801 reduced chronic disease, and early anti-fibrotic agent (nintedanib) intervention modified early disease severity. This murine model provides opportunities to identify pathways associated with persistent SARS-CoV-2 pulmonary disease and test countermeasures to ameliorate PASC.

show abstract

Pulmonary Sequelae at 4 Months After COVID-19 Infection: A Single-Centre Experience of a COVID Follow-Up Service

Abstract: Introduction: At the end of the first year of the COVID-19 pandemic, more than 78 million known survivors were recorded. The long-term pulmonary sequelae of COVID-19 remain unknown. Methods: We performed a retrospective analysis of a post-COVID follow-up service to

Cited by 26 publications

References 36 publications

A model of persistent post SARS-CoV-2 induced lung disease for target identification and testing of therapeutic strategies

A model of persistent post SARS-CoV-2 induced lung disease for target identification and testing of therapeutic strategies

Proposed subtypes of post‐COVID‐19 syndrome (or long‐COVID) and their respective potential therapies

SARS-CoV-2 infection produces chronic pulmonary epithelial and immune cell dysfunction with fibrosis in mice

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