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1.
Chest ; 161(1): 169-178, 2022 01.
Article in English | MEDLINE | ID: covidwho-1616416

ABSTRACT

The COVID-19 pandemic has caused acute lung injury in millions of individuals worldwide. Some patients develop COVID-related acute respiratory distress syndrome (CARDS) and cannot be liberated from mechanical ventilation. Others may develop post-COVID fibrosis, resulting in substantial disability and need for long-term supplemental oxygen. In both of these situations, treatment teams often inquire about the possibility of lung transplantation. In fact, lung transplantation has been successfully employed for both CARDS and post-COVID fibrosis in a limited number of patients worldwide. Lung transplantation after COVID infection presents a number of unique challenges that transplant programs must consider. In those with severe CARDS, the inability to conduct proper psychosocial evaluation and pretransplantation education, marked deconditioning from critical illness, and infectious concerns regarding viral reactivation are major hurdles. In those with post-COVID fibrosis, our limited knowledge about the natural history of recovery after COVID-19 infection is problematic. Increased knowledge of the likelihood and degree of recovery after COVID-19 acute lung injury is essential for appropriate decision-making with regard to transplantation. Transplant physicians must weigh the risks and benefits of lung transplantation differently in a post-COVID fibrosis patient who is likely to remain stable or gradually improve in comparison with a patient with a known progressive fibrosing interstitial lung disease (fILD). Clearly lung transplantation can be a life-saving therapeutic option for some patients with severe lung injury from COVID-19 infection. In this review, we discuss how lung transplant providers from a number of experienced centers approach lung transplantation for CARDS or post-COVID fibrosis.


Subject(s)
COVID-19/surgery , Lung Transplantation , Pneumonia, Viral/surgery , Pulmonary Fibrosis/surgery , Humans , Pandemics , Pneumonia, Viral/virology , Pulmonary Fibrosis/virology , SARS-CoV-2
2.
Medicine (Baltimore) ; 100(51): e28282, 2021 Dec 23.
Article in English | MEDLINE | ID: covidwho-1595309

ABSTRACT

BACKGROUND: Novel coronavirus disease (COVID-19) is a kind of pulmonary inflammation induced by New Coronavirus. It seriously threatens people's health and safety. Clinical studies have found that some patients have different degrees of inflammation after discharge from hospital, especially in patients with severe inflammatory lung fibrosis. Early combination of Chinese medicine and modern medicine has important clinical significance. There are still many deficiencies in the current research. We studied the effectiveness of the combination of traditional Chinese medicine and modern medicine in the treatment of pulmonary fibrosis caused by COVID-19, and proposed a network meta-analysis (NMA) scheme. METHODS: According to the search strategy, we will search Chinese and English databases to collect all randomized controlled trials of traditional Chinese medicine combined with modern drugs or only using traditional Chinese medicine for new coronavirus-19-induced pulmonary fibrosis between December 1, 2019 and November 15, 2021. First, the literature was screened according to the eligibility criteria, endnotex9 was used to manage the literature, and the Cochrane Collaboration's tool was used to assess the quality of the included literature. Revman 5.3, Stata 14.2, and gemtc14.3 meta-analysis software was then used for data processing and analysis, and the grading of recommendations assessment will be used to develop and evaluate a hierarchy for classifying the quality of evidence for NMA. RESULTS: Through the analysis, the ranking of efficacy and safety of various treatments for pulmonary fibrosis caused by COVID-19 will be drawn, thus providing stronger evidence support for the choice of clinical treatment methods. CONCLUSION: Traditional Chinese medicine (TCM) combined with modern drugs has played a positive role in the treatment of pulmonary fibrosis caused by COVID-19, and this study may provide more references for the clinical medication of pulmonary fibrosis caused by COVID-19. INPLASY REGISTRATION NUMBER: INPLASY2021110061.


Subject(s)
COVID-19 , Drugs, Chinese Herbal , Pulmonary Fibrosis , Bayes Theorem , COVID-19/drug therapy , Drugs, Chinese Herbal/therapeutic use , Humans , Medicine, Chinese Traditional , Meta-Analysis as Topic , Network Meta-Analysis , Pulmonary Fibrosis/drug therapy , Pulmonary Fibrosis/virology , Randomized Controlled Trials as Topic , Treatment Outcome
3.
Chest ; 161(1): 169-178, 2022 01.
Article in English | MEDLINE | ID: covidwho-1540448

ABSTRACT

The COVID-19 pandemic has caused acute lung injury in millions of individuals worldwide. Some patients develop COVID-related acute respiratory distress syndrome (CARDS) and cannot be liberated from mechanical ventilation. Others may develop post-COVID fibrosis, resulting in substantial disability and need for long-term supplemental oxygen. In both of these situations, treatment teams often inquire about the possibility of lung transplantation. In fact, lung transplantation has been successfully employed for both CARDS and post-COVID fibrosis in a limited number of patients worldwide. Lung transplantation after COVID infection presents a number of unique challenges that transplant programs must consider. In those with severe CARDS, the inability to conduct proper psychosocial evaluation and pretransplantation education, marked deconditioning from critical illness, and infectious concerns regarding viral reactivation are major hurdles. In those with post-COVID fibrosis, our limited knowledge about the natural history of recovery after COVID-19 infection is problematic. Increased knowledge of the likelihood and degree of recovery after COVID-19 acute lung injury is essential for appropriate decision-making with regard to transplantation. Transplant physicians must weigh the risks and benefits of lung transplantation differently in a post-COVID fibrosis patient who is likely to remain stable or gradually improve in comparison with a patient with a known progressive fibrosing interstitial lung disease (fILD). Clearly lung transplantation can be a life-saving therapeutic option for some patients with severe lung injury from COVID-19 infection. In this review, we discuss how lung transplant providers from a number of experienced centers approach lung transplantation for CARDS or post-COVID fibrosis.


Subject(s)
COVID-19/surgery , Lung Transplantation , Pneumonia, Viral/surgery , Pulmonary Fibrosis/surgery , Humans , Pandemics , Pneumonia, Viral/virology , Pulmonary Fibrosis/virology , SARS-CoV-2
4.
Clin Chem Lab Med ; 60(3): 307-316, 2022 02 23.
Article in English | MEDLINE | ID: covidwho-1518385

ABSTRACT

Pulmonary fibrosis (PF), a pathological outcome of chronic and acute interstitial lung diseases associated to compromised wound healing, is a key component of the "post-acute COVID-19 syndrome" that may severely complicate patients' clinical course. Although inconclusive, available data suggest that more than a third of hospitalized COVID-19 patients develop lung fibrotic abnormalities after their discharge from hospital. The pathogenesis of PF in patients recovering from a severe acute case of COVID-19 is complex, and several hypotheses have been formulated to explain its development. An analysis of the data that is presently available suggests that biomarkers of susceptibility could help to identify subjects with increased probability of developing PF and may represent a means to personalize the management of COVID-19's long-term effects. Our review highlights the importance of both patient-related and disease-related contributing risk factors for PF in COVID-19 survivors and makes it definitely clear the possible use of acute phase and follow-up biomarkers for identifying the patients at greatest risk of developing this disease.


Subject(s)
COVID-19 , Pulmonary Fibrosis , Biomarkers , COVID-19/complications , Humans , Pulmonary Fibrosis/virology , Survivors
5.
Thorax ; 76(12): 1242-1245, 2021 12.
Article in English | MEDLINE | ID: covidwho-1518155

ABSTRACT

The risk factors for development of fibrotic-like radiographic abnormalities after severe COVID-19 are incompletely described and the extent to which CT findings correlate with symptoms and physical function after hospitalisation remains unclear. At 4 months after hospitalisation, fibrotic-like patterns were more common in those who underwent mechanical ventilation (72%) than in those who did not (20%). We demonstrate that severity of initial illness, duration of mechanical ventilation, lactate dehydrogenase on admission and leucocyte telomere length are independent risk factors for fibrotic-like radiographic abnormalities. These fibrotic-like changes correlate with lung function, cough and measures of frailty, but not with dyspnoea.


Subject(s)
COVID-19 , Pulmonary Fibrosis , Telomere , COVID-19/complications , Dyspnea , Fibrosis , Humans , Pulmonary Fibrosis/diagnostic imaging , Pulmonary Fibrosis/genetics , Pulmonary Fibrosis/virology , Telomere/genetics
6.
Int J Mol Sci ; 22(14)2021 Jul 13.
Article in English | MEDLINE | ID: covidwho-1314665

ABSTRACT

Lung fibrosis has specific computed tomography (CT) findings and represents a common finding in advanced COVID-19 pneumonia whose reversibility has been poorly investigated. The aim of this study was to quantify the extension of collagen deposition and aeration in postmortem cryobiopsies of critically ill COVID-19 patients and to describe the correlations with qualitative and quantitative analyses of lung CT. Postmortem transbronchial cryobiopsy samples were obtained, formalin fixed, paraffin embedded and stained with Sirius red to quantify collagen deposition, defining fibrotic samples as those with collagen deposition above 10%. Lung CT images were analyzed qualitatively with a radiographic score and quantitatively with computer-based analysis at the lobe level. Thirty samples from 10 patients with COVID-19 pneumonia deceased during invasive mechanical ventilation were included in this study. The median [interquartile range] percent collagen extension was 6.8% (4.6-16.2%). In fibrotic compared to nonfibrotic samples, the qualitative score was higher (260 (250-290) vs. 190 (120-270), p = 0.036) while the gas fraction was lower (0.46 (0.32-0.47) vs. 0.59 (0.37-0.68), p = 0.047). A radiographic score above 230 had 100% sensitivity (95% confidence interval, CI: 66.4% to 100%) and 66.7% specificity (95% CI: 41.0% to 92.3%) to detect fibrotic samples, while a gas fraction below 0.57 had 100% sensitivity (95% CI: 66.4% to 100%) and 57.1% specificity (95% CI: 26.3% to 88.0%). In COVID-19 pneumonia, qualitative and quantitative analyses of lung CT images have high sensitivity but moderate to low specificity to detect histopathological fibrosis. Pseudofibrotic CT findings do not always correspond to increased collagen deposition.


Subject(s)
COVID-19/complications , Collagen/metabolism , Pulmonary Fibrosis/diagnosis , SARS-CoV-2/isolation & purification , Tomography, X-Ray Computed/methods , Aged , Autopsy , COVID-19/epidemiology , COVID-19/virology , Female , Humans , Italy/epidemiology , Male , Middle Aged , Pulmonary Fibrosis/diagnostic imaging , Pulmonary Fibrosis/metabolism , Pulmonary Fibrosis/virology , Retrospective Studies
7.
Respir Res ; 22(1): 203, 2021 Jul 09.
Article in English | MEDLINE | ID: covidwho-1300252

ABSTRACT

BACKGROUND: Thousands of Coronavirus Disease 2019 (COVID-19) patients have been discharged from hospitals Persistent follow-up studies are required to evaluate the prevalence of post-COVID-19 fibrosis. METHODS: This study involves 462 laboratory-confirmed patients with COVID-19 who were admitted to Shenzhen Third People's Hospital from January 11, 2020 to April 26, 2020. A total of 457 patients underwent thin-section chest CT scans during the hospitalization or after discharge to identify the pulmonary lesion. A total of 287 patients were followed up from 90 to 150 days after the onset of the disease, and lung function tests were conducted about three months after the onset. The risk factors affecting the persistence of pulmonary fibrosis were identified through regression analysis and the prediction model of the persistence of pulmonary fibrosis was established. RESULTS: Parenchymal bands, irregular interfaces, reticulation and traction bronchiectasis were the most common CT features in all COVID-19 patients. During the 0-30, 31-60, 61-90, 91-120 and > 120 days after onset, 86.87%, 74.40%, 79.56%, 68.12% and 62.03% patients developed with pulmonary fibrosis and 4.53%, 19.61%, 18.02%, 38.30% and 48.98% patients reversed pulmonary fibrosis, respectively. It was observed that Age, BMI, Fever, and Highest PCT were predictive factors for sustaining fibrosis even after 90 days from onset. A predictive model of the persistence with pulmonary fibrosis was developed based-on the Logistic Regression method with an accuracy, PPV, NPV, Sensitivity and Specificity of the model of 76%, 71%, 79%, 67%, and 82%, respectively. More than half of the COVID-19 patients revealed abnormal conditions in lung function after 90 days from onset, and the ratio of abnormal lung function did not differ on a statistically significant level between the fibrotic and non-fibrotic groups. CONCLUSIONS: Persistent pulmonary fibrosis was more likely to develop in patients with older age, higher BMI, severe/critical condition, fever, a longer viral clearance time, pre-existing disease and delayed hospitalization. Fibrosis developed in COVID-19 patients could be reversed in about a third of the patients after 120 days from onset. The pulmonary function of less than half of COVID-19 patients could turn to normal condition after three months from onset. An effective prediction model with an average area under the curve (AUC) of 0.84 was established to predict the persistence of pulmonary fibrosis in COVID-19 patients for early diagnosis.


Subject(s)
COVID-19/virology , Lung/virology , Patient Discharge , Pulmonary Fibrosis/virology , SARS-CoV-2/pathogenicity , Adolescent , Adult , COVID-19/complications , COVID-19/diagnosis , China , Female , Host-Pathogen Interactions , Humans , Lung/diagnostic imaging , Lung/physiopathology , Male , Middle Aged , Prognosis , Pulmonary Fibrosis/diagnostic imaging , Pulmonary Fibrosis/physiopathology , Respiratory Function Tests , Time Factors , Tomography, X-Ray Computed , Young Adult
9.
Crit Care ; 25(1): 224, 2021 06 30.
Article in English | MEDLINE | ID: covidwho-1286832

ABSTRACT

BACKGROUND: Previous studies reporting the causes of death in patients with severe COVID-19 have provided conflicting results. The objective of this study was to describe the causes and timing of death in patients with severe COVID-19 admitted to the intensive care unit (ICU). METHODS: We performed a retrospective study in eight ICUs across seven French hospitals. All consecutive adult patients (aged ≥ 18 years) admitted to the ICU with PCR-confirmed SARS-CoV-2 infection and acute respiratory failure were included in the analysis. The causes and timing of ICU deaths were reported based on medical records. RESULTS: From March 1, 2020, to April 28, 287 patients were admitted to the ICU for SARS-CoV-2 related acute respiratory failure. Among them, 93 patients died in the ICU (32%). COVID-19-related multiple organ dysfunction syndrome (MODS) was the leading cause of death (37%). Secondary infection-related MODS accounted for 26% of ICU deaths, with a majority of ventilator-associated pneumonia. Refractory hypoxemia/pulmonary fibrosis was responsible for death in 19% of the cases. Fatal ischemic events (venous or arterial) occurred in 13% of the cases. The median time from ICU admission to death was 15 days (25th-75th IQR, 7-27 days). COVID-19-related MODS had a median time from ICU admission to death of 14 days (25th-75th IQR: 7-19 days), while only one death had occurred during the first 3 days since ICU admission. CONCLUSIONS: In our multicenter observational study, COVID-19-related MODS and secondary infections were the two leading causes of death, among severe COVID-19 patients admitted to the ICU.


Subject(s)
COVID-19/mortality , Multiple Organ Failure/mortality , Pneumonia, Viral/mortality , Adult , Cause of Death , Female , Hospital Mortality , Humans , Hypoxia/mortality , Hypoxia/virology , Intensive Care Units , Ischemia/mortality , Ischemia/virology , Male , Multiple Organ Failure/virology , Pneumonia, Ventilator-Associated/mortality , Pneumonia, Ventilator-Associated/virology , Pneumonia, Viral/virology , Pulmonary Fibrosis/mortality , Pulmonary Fibrosis/virology , Retrospective Studies , SARS-CoV-2
10.
Immunol Rev ; 302(1): 228-240, 2021 07.
Article in English | MEDLINE | ID: covidwho-1241009

ABSTRACT

The COVID-19 pandemic rapidly spread around the world following the first reports in Wuhan City, China in late 2019. The disease, caused by the novel SARS-CoV-2 virus, is primarily a respiratory condition that can affect numerous other bodily systems including the cardiovascular and gastrointestinal systems. The disease ranges in severity from asymptomatic through to severe acute respiratory distress requiring intensive care treatment and mechanical ventilation, which can lead to respiratory failure and death. It has rapidly become evident that COVID-19 patients can develop features of interstitial pulmonary fibrosis, which in many cases persist for as long as we have thus far been able to follow the patients. Many questions remain about how such fibrotic changes occur within the lung of COVID-19 patients, whether the changes will persist long term or are capable of resolving, and whether post-COVID-19 pulmonary fibrosis has the potential to become progressive, as in other fibrotic lung diseases. This review brings together our existing knowledge on both COVID-19 and pulmonary fibrosis, with a particular focus on lung epithelial cells and fibroblasts, in order to discuss common pathways and processes that may be implicated as we try to answer these important questions in the months and years to come.


Subject(s)
COVID-19/pathology , Epithelial Cells/pathology , Fibroblasts/pathology , Pulmonary Fibrosis/pathology , Pulmonary Fibrosis/virology , Respiratory Mucosa/pathology , COVID-19/complications , Humans , SARS-CoV-2
11.
Cells ; 10(5)2021 05 14.
Article in English | MEDLINE | ID: covidwho-1234672

ABSTRACT

To date, more than 100 million people worldwide have recovered from COVID-19. Unfortunately, although the virus is eradicated in such patients, fibrotic irreversible interstitial lung disease (pulmonary fibrosis, PF) is clinically evident. Given the vast numbers of individuals affected, it is urgent to design a strategy to prevent a second wave of late mortality associated with COVID-19 PF as a long-term consequence of such a devastating pandemic. Available antifibrotic therapies, namely nintedanib and pirfenidone, might have a role in attenuating profibrotic pathways in SARS-CoV-2 infection but are not economically sustainable by national health systems and have critical adverse effects. It is our opinion that the mesenchymal stem cell secretome could offer a new therapeutic approach in treating COVID-19 fibrotic lungs through its anti-inflammatory and antifibrotic factors.


Subject(s)
Biological Factors/pharmacology , COVID-19/complications , Mesenchymal Stem Cells/metabolism , Pulmonary Fibrosis/drug therapy , Biological Factors/metabolism , Biological Factors/therapeutic use , COVID-19/drug therapy , COVID-19/economics , COVID-19/virology , Humans , Indoles/administration & dosage , Indoles/adverse effects , Indoles/economics , Lung/drug effects , Lung/pathology , Lung/virology , Pulmonary Fibrosis/economics , Pulmonary Fibrosis/virology , Pyridones/administration & dosage , Pyridones/adverse effects , Pyridones/economics , SARS-CoV-2/pathogenicity
12.
Sci Transl Med ; 12(574)2020 12 16.
Article in English | MEDLINE | ID: covidwho-1207479

ABSTRACT

Lung transplantation can potentially be a life-saving treatment for patients with nonresolving COVID-19-associated respiratory failure. Concerns limiting lung transplantation include recurrence of SARS-CoV-2 infection in the allograft, technical challenges imposed by viral-mediated injury to the native lung, and the potential risk for allograft infection by pathogens causing ventilator-associated pneumonia in the native lung. Additionally, the native lung might recover, resulting in long-term outcomes preferable to those of transplant. Here, we report the results of lung transplantation in three patients with nonresolving COVID-19-associated respiratory failure. We performed single-molecule fluorescence in situ hybridization (smFISH) to detect both positive and negative strands of SARS-CoV-2 RNA in explanted lung tissue from the three patients and in additional control lung tissue samples. We conducted extracellular matrix imaging and single-cell RNA sequencing on explanted lung tissue from the three patients who underwent transplantation and on warm postmortem lung biopsies from two patients who had died from COVID-19-associated pneumonia. Lungs from these five patients with prolonged COVID-19 disease were free of SARS-CoV-2 as detected by smFISH, but pathology showed extensive evidence of injury and fibrosis that resembled end-stage pulmonary fibrosis. Using machine learning, we compared single-cell RNA sequencing data from the lungs of patients with late-stage COVID-19 to that from the lungs of patients with pulmonary fibrosis and identified similarities in gene expression across cell lineages. Our findings suggest that some patients with severe COVID-19 develop fibrotic lung disease for which lung transplantation is their only option for survival.


Subject(s)
COVID-19/surgery , Lung Transplantation , Lung/surgery , Pulmonary Fibrosis/surgery , Adult , Aged, 80 and over , COVID-19/diagnosis , COVID-19/physiopathology , COVID-19/virology , COVID-19 Nucleic Acid Testing , Databases, Factual , Disease Progression , Female , Humans , In Situ Hybridization, Fluorescence , Lung/physiopathology , Lung/virology , Male , Middle Aged , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/physiopathology , Pulmonary Fibrosis/virology , RNA-Seq , Recovery of Function , Retrospective Studies , Severity of Illness Index , Single-Cell Analysis , Treatment Outcome
13.
High Blood Press Cardiovasc Prev ; 28(4): 373-381, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1205023

ABSTRACT

The aim of the study was to assess the short-term consequences of SARS-CoV-2-related pneumonia, also in relation to radiologic/laboratory/clinical indices of risk at baseline. This prospective follow-up cohort study included 94 patients with confirmed COVID-19 admitted to a medical ward at the Montichiari Hospital, Brescia, Italy from February 28th to April 30th, 2020. Patients had COVID-19 related pneumonia with respiratory failure. Ninety-four patients out of 193 survivors accepted to be re-evaluated after discharge, on average after 4 months. In » of the patients an evidence of pulmonary fibrosis was detected, as indicated by an altered diffusing capacity of the lung for carbon monoxide (DLCO); in 6-7% of patients the alteration was classified as of moderate/severe degree. We also evaluated quality of life thorough a structured questionnaire: 52% of the patients still lamented fatigue, 36% effort dyspnea, 10% anorexia, 14% dysgeusia or anosmia, 31% insomnia and 21% anxiety. Finally, we evaluated three prognostic indices (the Brixia radiologic score, the Charlson Comorbidity Index and the 4C mortality score) in terms of prediction of the clinical consequences of the disease. All of them significantly predicted the extent of short-term lung involvement. In conclusion, our study demonstrated that SARS-CoV-2-related pneumonia is associated to relevant short-term clinical consequences, both in terms of persistence of symptoms and in terms of impairment of DLCO (indicator of a possible development of pulmonary fibrosis); some severity indices of the disease may predict short-term clinical outcome. Further studies are needed to ascertain whether such manifestations may persist long-term.


Subject(s)
COVID-19/virology , Lung Diseases, Interstitial/virology , Lung/virology , Pulmonary Fibrosis/virology , SARS-CoV-2/pathogenicity , COVID-19/complications , COVID-19/diagnosis , Follow-Up Studies , Host-Pathogen Interactions , Humans , Italy , Lung/pathology , Lung/physiopathology , Lung Diseases, Interstitial/diagnosis , Lung Diseases, Interstitial/physiopathology , Prognosis , Prospective Studies , Pulmonary Diffusing Capacity , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/physiopathology , Quality of Life , Time Factors
14.
J Infect Dev Ctries ; 15(3): 360-365, 2021 Mar 31.
Article in English | MEDLINE | ID: covidwho-1175612

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus that causes coronavirus diseases 2019 (COVID-19). The SARS-CoV-2 is very contagious and nobody is known to be immune to it. The post-infected lung would leave a scar known as fibrosis, a scar tissue. A study from Wuhan, China suggested the development of fibrosis, though it was too early to label these lung changes as irreversible fibrosis in a time range of 3 weeks. The occurrence of fibrosis indicates a chronic infection which greatly contributes to the hallmark symptom of COVID-19 induced ARDS such as shortness of breath and chest pain. However, many of those studies have not yet explained the condition of the patient's lung after total recovery from the COVID-19. This report demonstrates the clinical symptoms, chest CT scan, spirometry, and blood gas analysis of patient after total recovery from the COVID-19 with appearance lung fibrosis.


Subject(s)
COVID-19/complications , Lung/pathology , Lung/virology , Pulmonary Fibrosis/virology , Blood Gas Analysis , COVID-19/epidemiology , COVID-19/physiopathology , China/epidemiology , Chronic Disease/epidemiology , Disease Progression , Humans , Lung/diagnostic imaging , Male , Middle Aged , Pulmonary Fibrosis/diagnostic imaging , Pulmonary Fibrosis/epidemiology , Spirometry , Thorax/diagnostic imaging , Tomography, X-Ray Computed
15.
Eur Rev Med Pharmacol Sci ; 25(6): 2748-2751, 2021 Mar.
Article in English | MEDLINE | ID: covidwho-1173126

ABSTRACT

COVID-19 is an acute respiratory infectious disease caused by SARS-COV 2 (Severe Acute Respiratory Syndrome Coronavirus) that has become a global pandemic. COVID-19 mainly causes the respiratory complications of Acute Respiratory Distress Syndrome (ARDS), cytokine storm, and severe immune disruptions. The assays depict that though people recuperate from COVID-19, there are still symptoms that persists in the body causing discomfort, which is the consequence of the viral infection due to severe immune disruptions. Upon various difficulties of post COVID-19, the pulmonary fibrosis is the stumbling block in the lungs causing severe damage. In this review, we have shown the effectiveness and importance of the Hepatocyte Growth Factor (HGF) secreted by Mesenchymal Stem Cell (MSC) therapy on selective stoppage of the Transforming Growth Factor-Beta (TGF-ß) signalling pathway by causing immunomodulatory effects that ameliorate the pulmonary fibrosis through paracrine signalling. However, more pilot studies have to be carried out to determine the efficacy and outcomes of the re-emerging complication.


Subject(s)
COVID-19/epidemiology , Mesenchymal Stem Cell Transplantation/methods , Mesenchymal Stem Cells/cytology , Pulmonary Fibrosis/therapy , Pulmonary Fibrosis/virology , COVID-19/transmission , COVID-19/virology , Global Health , Humans , Pulmonary Fibrosis/epidemiology , SARS-CoV-2/isolation & purification
16.
Stem Cells ; 39(6): 707-722, 2021 06.
Article in English | MEDLINE | ID: covidwho-1121521

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic has grown to be a global public health crisis with no safe and effective treatments available yet. Recent findings suggest that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the coronavirus pathogen that causes COVID-19, could elicit a cytokine storm that drives edema, dysfunction of the airway exchange, and acute respiratory distress syndrome in the lung, followed by acute cardiac injury and thromboembolic events leading to multiorgan failure and death. Mesenchymal stem cells (MSCs), owing to their powerful immunomodulatory abilities, have the potential to attenuate the cytokine storm and have therefore been proposed as a potential therapeutic approach for which several clinical trials are underway. Given that intravenous infusion of MSCs results in a significant trapping in the lung, MSC therapy could directly mitigate inflammation, protect alveolar epithelial cells, and reverse lung dysfunction by normalizing the pulmonary microenvironment and preventing pulmonary fibrosis. In this review, we present an overview and perspectives of the SARS-CoV-2 induced inflammatory dysfunction and the potential of MSC immunomodulation for the prevention and treatment of COVID-19 related pulmonary disease.


Subject(s)
COVID-19/immunology , Cytokine Release Syndrome/immunology , Mesenchymal Stem Cells/immunology , SARS-CoV-2/immunology , COVID-19/therapy , COVID-19/virology , Cytokine Release Syndrome/therapy , Cytokine Release Syndrome/virology , Humans , Immunomodulation , Lung/immunology , Lung/pathology , Lung/virology , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells/virology , Pandemics , Pulmonary Fibrosis/immunology , Pulmonary Fibrosis/therapy , Pulmonary Fibrosis/virology , Respiratory Distress Syndrome/immunology , Respiratory Distress Syndrome/therapy , Respiratory Distress Syndrome/virology , SARS-CoV-2/genetics
17.
Travel Med Infect Dis ; 40: 101995, 2021.
Article in English | MEDLINE | ID: covidwho-1101526

ABSTRACT

BACKGROUND: There is emerging evidence of long-term sequelae in a considerable proportion of COVID-19 patients after recovery and the spectrum and severity of such sequelae should be systematically reviewed. This review aims to evaluate the available evidence of all intermediate and long-term COVID-19 sequelae affecting formerly healthy adults. METHODS: A systematic literature search of Embase, WHO, Scopus, Pubmed, Litcovid, bioRxiv and medRxiv was conducted with a cutoff date of the 17th September 2020 according to PRISMA guidelines and registered in PROSPERO (CRD42020208725). Search terms included "COVID-19", "coronavirus disease 2019", "SARS-CoV-2", "sequelae" and "consequence*". Publications on adult participants, with a confirmed SARS-CoV-2 infection were included. Elderly (>50 years old) and children (<18 years old) were excluded. Bias assessment was performed using a modified Newcastle-Ottawa Scale. RESULTS: A total of 31 papers were included. Study types included prospective and retrospective cohort studies, cross-sectional studies and case reports. Sequelae persistence since infection spanned 14 days to three months. Sequelae included persistent fatigue (39-73% of assessed persons), breathlessness (39-74%), decrease in quality of life (44-69%), impaired pulmonary function, abnormal CT findings including pulmonary fibrosis (39-83%), evidence of peri-/perimyo-/myocarditis (3-26%), changes in microstructural and functional brain integrity with persistent neurological symptoms (55%), increased incidence of psychiatric diagnoses (5.8% versus 2.5-3.4% in controls), incomplete recovery of olfactory and gustatory dysfunction (33-36% of evaluated persons). CONCLUSIONS: A variety of organ systems are affected by COVID-19 in the intermediate and longer-term after recovery. Main sequelae include post-infectious fatigue, persistent reduced lung function and carditis. Careful follow-up post COVID 19 is indicated to assess and mitigate possible organ damage and preserve life quality.


Subject(s)
COVID-19/physiopathology , Aged , COVID-19/diagnostic imaging , COVID-19/epidemiology , Databases, Factual , Dyspnea/virology , Fatigue , Humans , Lung/diagnostic imaging , Lung/physiopathology , Lung/virology , Middle Aged , Myocarditis/virology , Pulmonary Fibrosis/virology , Quality of Life , SARS-CoV-2/isolation & purification
18.
Am J Physiol Lung Cell Mol Physiol ; 320(2): L257-L265, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-1088310

ABSTRACT

The novel SARS-CoV-2 coronavirus, which is responsible for COVID-19 disease, was first reported in Wuhan, China, in December of 2019. The virus rapidly spread, and the World Health Organization declared a pandemic by March 2020. With millions of confirmed cases worldwide, there is growing concern and considerable debate regarding the potential for coronavirus infection to contribute to an appreciable burden of chronic respiratory symptoms or fibrotic disease among recovered individuals. Because the first case of COVID-19 was documented less than one year ago, data regarding long-term clinical outcomes are not yet available, and predictions for long-term outcome are speculative at best. However, due to the staggering number of cases and the severity of disease in many individuals, there is a critical need to consider the potential long-term implications of COVID-19. This review examines current basic and clinical data regarding fibrogenic mechanisms of viral injury in the context of SARS-CoV-2. Several intersecting mechanisms between coronavirus infection and fibrotic pathways are discussed to highlight factors and processes that may be targetable to improve patient outcome. Reports of post-infection sequelae from previous coronavirus outbreaks are presented toward the goal of improved recognition of potential contributing risk factors for fibrotic disease.


Subject(s)
COVID-19/complications , Pandemics , Pulmonary Fibrosis/etiology , SARS-CoV-2 , Age Factors , Aged , Aged, 80 and over , COVID-19/epidemiology , COVID-19/virology , Cytokines/physiology , Host Microbial Interactions/physiology , Humans , Inflammation/etiology , Inflammation/virology , Pulmonary Fibrosis/virology , Respiration, Artificial/adverse effects , Respiratory Distress Syndrome/complications , Respiratory Distress Syndrome/etiology , Risk Factors , SARS-CoV-2/pathogenicity , SARS-CoV-2/physiology , Signal Transduction , Survivors
19.
Sci Adv ; 7(1)2021 01.
Article in English | MEDLINE | ID: covidwho-1066781

ABSTRACT

Despite past extensive studies, the mechanisms underlying pulmonary fibrosis (PF) still remain poorly understood. Here, we demonstrated that lungs originating from different types of patients with PF, including coronavirus disease 2019, systemic sclerosis-associated interstitial lung disease, and idiopathic PF, and from mice following bleomycin (BLM)-induced PF are characterized by the altered methyl-CpG-binding domain 2 (MBD2) expression in macrophages. Depletion of Mbd2 in macrophages protected mice against BLM-induced PF. Mbd2 deficiency significantly attenuated transforming growth factor-ß1 (TGF-ß1) production and reduced M2 macrophage accumulation in the lung following BLM induction. Mechanistically, Mbd2 selectively bound to the Ship promoter in macrophages, by which it repressed Ship expression and enhanced PI3K/Akt signaling to promote the macrophage M2 program. Therefore, intratracheal administration of liposomes loaded with Mbd2 siRNA protected mice from BLM-induced lung injuries and fibrosis. Together, our data support the possibility that MBD2 could be a viable target against PF in clinical settings.


Subject(s)
COVID-19/metabolism , DNA-Binding Proteins/metabolism , Macrophages/metabolism , Pulmonary Fibrosis/metabolism , Animals , Bleomycin/pharmacology , Carcinoma, Non-Small-Cell Lung/metabolism , Fibrosis , Gene Expression Profiling , Gene Expression Regulation , Humans , Liposomes/chemistry , Lung Diseases, Interstitial/metabolism , Lung Neoplasms/metabolism , Macrophages/virology , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Pulmonary Fibrosis/virology , RNA, Small Interfering/metabolism , Scleroderma, Systemic/metabolism , Signal Transduction , Transforming Growth Factor beta1/metabolism
20.
Am J Physiol Lung Cell Mol Physiol ; 320(2): L257-L265, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-999315

ABSTRACT

The novel SARS-CoV-2 coronavirus, which is responsible for COVID-19 disease, was first reported in Wuhan, China, in December of 2019. The virus rapidly spread, and the World Health Organization declared a pandemic by March 2020. With millions of confirmed cases worldwide, there is growing concern and considerable debate regarding the potential for coronavirus infection to contribute to an appreciable burden of chronic respiratory symptoms or fibrotic disease among recovered individuals. Because the first case of COVID-19 was documented less than one year ago, data regarding long-term clinical outcomes are not yet available, and predictions for long-term outcome are speculative at best. However, due to the staggering number of cases and the severity of disease in many individuals, there is a critical need to consider the potential long-term implications of COVID-19. This review examines current basic and clinical data regarding fibrogenic mechanisms of viral injury in the context of SARS-CoV-2. Several intersecting mechanisms between coronavirus infection and fibrotic pathways are discussed to highlight factors and processes that may be targetable to improve patient outcome. Reports of post-infection sequelae from previous coronavirus outbreaks are presented toward the goal of improved recognition of potential contributing risk factors for fibrotic disease.


Subject(s)
COVID-19/complications , Pandemics , Pulmonary Fibrosis/etiology , SARS-CoV-2 , Age Factors , Aged , Aged, 80 and over , COVID-19/epidemiology , COVID-19/virology , Cytokines/physiology , Host Microbial Interactions/physiology , Humans , Inflammation/etiology , Inflammation/virology , Pulmonary Fibrosis/virology , Respiration, Artificial/adverse effects , Respiratory Distress Syndrome/complications , Respiratory Distress Syndrome/etiology , Risk Factors , SARS-CoV-2/pathogenicity , SARS-CoV-2/physiology , Signal Transduction , Survivors
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