SARS-CoV-2 Infects Human Engineered Heart Tissues and Models COVID-19 Myocarditis

Bailey, Adam L.; Dmytrenko, Oleksandr; Bredemeyer, Andrea L.; Ma, Pan; Liu, Jing; Penna, Vinay; Winkler, Emma S.; Sviben, Sanja; Brooks, Erin G.; Nair, Ajith; Heck, Kent A.; Rali, Aniket S; Simpson, Leo; Saririan, Mehrdad; Hobohm, Dan; Stump, W. Tom; Fitzpatrick, James A.J.; Xie, Xuping; Zhang, Xianwen; Shi, Pei–Yong; Hinson, J. Travis; Gi, Weng‐Tein; Schmidt, Constanze; Leuschner, Florian; Lin, Chieh‐Yu; Diamond, Michael S.; Greenberg, Michael J.; Lavine, Kory J.

doi:10.1016/j.jacbts.2021.01.002

Cited by 145 publications

(190 citation statements)

References 41 publications

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“…It is worth mentioning that, except alveoli, which is widely known as the target tissue, cardiomyocyte can be infected as well. Researches proved that SARS-CoV-2 can directly infect human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) as well as an engineered heart tissue (EHT), in cellular and organ level respectively, suggesting that the virus can replicate rapidly in the cardiomyocytes, infecting other cardiomyocytes, contributing to cardiomyocyte cell death, myocardial inflammation and even heart failure ( Sharma et al, 2020 ; Bailey et al, 2021 ).…”

Section: Virological Characteristics Of Covid-19mentioning

confidence: 99%

Pulmonary Edema in COVID-19 Patients: Mechanisms and Treatment Potential

et al. 2021

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COVID-19 mortality is primarily driven by abnormal alveolar fluid metabolism of the lung, leading to fluid accumulation in the alveolar airspace. This condition is generally referred to as pulmonary edema and is a direct consequence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. There are multiple potential mechanisms leading to pulmonary edema in severe Coronavirus Disease (COVID-19) patients and understanding of those mechanisms may enable proper management of this condition. Here, we provide a perspective on abnormal lung humoral metabolism of pulmonary edema in COVID-19 patients, review the mechanisms by which pulmonary edema may be induced in COVID-19 patients, and propose putative drug targets that may be of use in treating COVID-19. Among the currently pursued therapeutic strategies against COVID-19, little attention has been paid to abnormal lung humoral metabolism. Perplexingly, successful balance of lung humoral metabolism may lead to the reduction of the number of COVID-19 death limiting the possibility of healthcare services with insufficient capacity to provide ventilator-assisted respiration.

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Section: Virological Characteristics Of Covid-19mentioning

confidence: 99%

Pulmonary Edema in COVID-19 Patients: Mechanisms and Treatment Potential

et al. 2021

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“…Various cardiac cells express the ACE2 receptor and could be, therefore, targets for SARS-CoV2 infection, including cardiomyocytes, cardiac fibroblasts, pericytes, and possibly endothelial cells (but the latter is controversial) [124,125]. Recent studies using electron microscopy, RNA sequencing, and direct infection of pluripotent stem-cell-derived cardiomyocytes, as well as human engineered heart tissue, have definitely proven the capacity of SARS-CoV2 to infect, replicate, and induce cell death in cardiomyocytes [126]. In spite of this evidence, the actual incidence of typical myocarditis (as diagnosed by the presence of at least seven CD3-positive T-lymphocytes/mm 2 ) in COVID-19 is extremely uncommon, occurring in only 4.5% of highly selected cases undergoing autopsy or endomyocardial biopsy (EMB) [124].…”

Section: Myocardial Inflammationmentioning

confidence: 99%

The Right Ventricle in COVID-19

Bonnemain

Ltaief

Liaudet

2021

JCM

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Infection with the novel severe acute respiratory coronavirus-2 (SARS-CoV2) results in COVID-19, a disease primarily affecting the respiratory system to provoke a spectrum of clinical manifestations, the most severe being acute respiratory distress syndrome (ARDS). A significant proportion of COVID-19 patients also develop various cardiac complications, among which dysfunction of the right ventricle (RV) appears particularly common, especially in severe forms of the disease, and which is associated with a dismal prognosis. Echocardiographic studies indeed reveal right ventricular dysfunction in up to 40% of patients, a proportion even greater when the RV is explored with strain imaging echocardiography. The pathophysiological mechanisms of RV dysfunction in COVID-19 include processes increasing the pulmonary vascular hydraulic load and others reducing RV contractility, which precipitate the acute uncoupling of the RV with the pulmonary circulation. Understanding these mechanisms provides the fundamental basis for the adequate therapeutic management of RV dysfunction, which incorporates protective mechanical ventilation, the prevention and treatment of pulmonary vasoconstriction and thrombotic complications, as well as the appropriate management of RV preload and contractility. This comprehensive review provides a detailed update of the evidence of RV dysfunction in COVID-19, its pathophysiological mechanisms, and its therapy.

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“…The COVID-19 pandemic is a global health emergency caused by the severe acute respiratory syndrome virus 2 (SARS-CoV-2), a virus from the genus Betacoronavirus and family Coronaviridae [ 1 , 2 ]. Human patient data suggest that SARS-CoV-2 may be able to infect several organs in addition to the lungs, including the heart, kidneys, and brain [ 3 , 4 , 5 , 6 , 7 , 8 ]. Infection of the male genital tract (MGT) has been reported for a variety of viruses, including filoviruses (Ebola and Marburg viruses), flaviviruses (Zika virus), and paramyxoviruses (mumps virus), with implications for sexual transmission, persistence, fertility, and testicular health [ 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

SARS-CoV-2 Infects Hamster Testes

et al. 2021

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The COVID-19 pandemic continues to affect millions of people worldwide. Although SARS-CoV-2 is a respiratory virus, there is growing concern that the disease could cause damage and pathology outside the lungs, including in the genital tract. Studies suggest that SARS-CoV-2 infection can damage the testes and reduce testosterone levels, but the underlying mechanisms are unknown and evidence of virus replication in testicular cells is lacking. We infected golden Syrian hamsters intranasally, a model for mild human COVID-19, and detected viral RNA in testes samples without histopathological changes up to one month post-infection. Using an ex vivo infection model, we detected SARS-CoV-2 replication in hamster testicular cells. Taken together, our data raise the possibility that testes damage observed in severe cases of COVID-19 could be partly explained by direct SARS-CoV-2 infection of the testicular cells.

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SARS-CoV-2 Infects Human Engineered Heart Tissues and Models COVID-19 Myocarditis

Abstract: Visual Abstract

Cited by 145 publications

References 41 publications

Pulmonary Edema in COVID-19 Patients: Mechanisms and Treatment Potential

Pulmonary Edema in COVID-19 Patients: Mechanisms and Treatment Potential

The Right Ventricle in COVID-19

SARS-CoV-2 Infects Hamster Testes

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