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First Documentation of Persistent SARS-Cov-2 Infection Presenting With Late Acute Severe Myocarditis.

ABSTRACT: A 64-year-old man presented with severe myocarditis 6 weeks after an initial almost asymptomatic severe acute respiratory syndrome coronavirus-2 (SARS-CoV2) infection. He was found to have a persistent positive swab. Mechanisms explaining myocardial injury in patients with COVID-19 remains unclear, but this case suggests that severe acute myocarditis can develop in the late phase of COVID-19 infection, even after a symptom-free interval.

SUBMITTER: Pavon AG

PROVIDER: S-EPMC7834643 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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First Documentation of Persistent SARS-Cov-2 Infection Presenting With Late Acute Severe Myocarditis.

Pavon Anna Giulia AG Meier David D Samim Daryoush D Rotzinger David C DC Fournier Stephane S Marquis Patrick P Monney Pierre P Muller Olivier O Schwitter Juerg J

The Canadian journal of cardiology 20200606 8

A 64-year-old man presented with severe myocarditis 6 weeks after an initial almost asymptomatic severe acute respiratory syndrome coronavirus-2 (SARS-CoV2) infection. He was found to have a persistent positive swab. Mechanisms explaining myocardial injury in patients with COVID-19 remains unclear, but this case suggests that severe acute myocarditis can develop in the late phase of COVID-19 infection, even after a symptom-free interval. ...[more]

PMID: 32522523

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Project description:BACKGROUND:Myocarditis is inflammation of the heart muscle that can follow various viral infections. Why children only rarely develop life-threatening acute viral myocarditis (AVM), given that the causal viral infections are common, is unknown. Genetic lesions might underlie such susceptibilities. Mouse genetic studies demonstrated that interferon (IFN)-?/? immunity defects increased susceptibility to virus-induced myocarditis. Moreover, variations in human TLR3, a potent inducer of IFNs, were proposed to underlie AVM. OBJECTIVES:This study sought to evaluate the hypothesis that human genetic factors may underlie AVM in previously healthy children. METHODS:We tested the role of TLR3-IFN immunity using human induced pluripotent stem cell-derived cardiomyocytes. We then performed whole-exome sequencing of 42 unrelated children with acute myocarditis (AM), some with proven viral causes. RESULTS:We found that TLR3- and STAT1-deficient cardiomyocytes were not more susceptible to Coxsackie virus B3 (CVB3) infection than control cells. Moreover, CVB3 did not induce IFN-?/? and IFN-?/?-stimulated genes in control cardiomyocytes. Finally, exogenous IFN-? did not substantially protect cardiomyocytes against CVB3. We did not observe a significant enrichment of rare variations in TLR3- or IFN-?/?-related genes. Surprisingly, we found that homozygous but not heterozygous rare variants in genes associated with inherited cardiomyopathies were significantly enriched in AM-AVM patients compared with healthy individuals (p = 2.22E-03) or patients with other diseases (p = 1.08E-04). Seven of 42 patients (16.7%) carried rare biallelic (homozygous or compound heterozygous) nonsynonymous or splice-site variations in 6 cardiomyopathy-associated genes (BAG3, DSP, PKP2, RYR2, SCN5A, or TNNI3). CONCLUSIONS:Previously silent recessive defects of the myocardium may predispose to acute heart failure presenting as AM, notably after common viral infections in children.

Dataset Information

First Documentation of Persistent SARS-Cov-2 Infection Presenting With Late Acute Severe Myocarditis.

Publications

First Documentation of Persistent SARS-Cov-2 Infection Presenting With Late Acute Severe Myocarditis.

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