A cross-sectional investigation of SARS-CoV-2 seroprevalence and associated risk factors in children and adolescents in the United States.

BACKGROUND: Pediatric SARS-CoV-2 data remain limited and seropositivity rates in children were reported as <1% early in the pandemic. Seroepidemiologic evaluation of SARS-CoV-2 in children in a major metropolitan region of the US was performed. METHODS: Children and adolescents ≤19 years were enrolled in a cross-sectional, observational study of SARS-CoV-2 seroprevalence from July-October 2020 in Northern Virginia, US. Demographic, health, and COVID-19 exposure information was collected, and blood analyzed for SARS-CoV-2 spike protein total antibody. Risk factors associated with SARS-CoV-2 seropositivity were analyzed. Orthogonal antibody testing was performed, and samples were evaluated for responses to different antigens. RESULTS: In 1038 children, the anti-SARS-CoV-2 total antibody positivity rate was 8.5%. After multivariate logistic regression, significant risk factors included Hispanic ethnicity, public or absent insurance, a history of COVID-19 symptoms, exposure to person with COVID-19, a household member positive for SARS-CoV-2 and multi-family or apartment dwelling without a private entrance. 66% of seropositive children had no symptoms of COVID-19. Secondary analysis included orthogonal antibody testing with assays for 1) a receptor binding domain specific antigen and 2) a nucleocapsid specific antigen had concordance rates of 80.5% and 79.3% respectively. CONCLUSIONS: A much higher burden of SARS-CoV-2 infection, as determined by seropositivity, was found in children than previously reported; this was also higher compared to adults in the same region at a similar time. Contrary to prior reports, we determined children shoulder a significant burden of COVID-19 infection. The role of children's disease transmission must be considered in COVID-19 mitigation strategies including vaccination.

Regional remodeling strain and its association with myocardial apoptosis after myocardial infarction in an ovine model.

OBJECTIVE: Progressive left ventricular remodeling after myocardial infarction has been viewed as an important contributor to progressive heart failure. The objective of this study was to investigate the relationship between myocardial apoptosis and strain during progressive cardiac remodeling. METHODS: Before creation of an anterolateral left ventricular infarction by ligation of diagonal arteries, 16 sonomicrometry transducers were placed in the left ventricular free wall of 8 sheep to assess regional deformation in the infarct, adjacent, and normally perfused remote myocardial regions over 8 weeks' duration. Hemodynamic, echocardiographic and sonomicrometric data were collected before infarction and then 30 minutes and 2, 6, and 8 weeks after infarction. At the end of the study, regional myocardial tissues were collected for apoptotic signaling proteins. RESULTS: At terminal study, an increase in left ventricular end-diastolic pressure of 8.1 +/- 0.1 mm Hg, a decrease in ejection fraction from 54.19% +/- 5.68% to 30.55% +/- 2.72%, and an end-diastolic volume increase of 46.08 +/- 5.02 mL as compared with the preinfarct values were observed. The fractional contraction at terminal study correlated with the relative abundance of apoptotic protein expressions: cytochrome c (r(2) = 0.02, P < .05), mitochondrial Bax (r(2) = 0.27, P < .05), caspase-3 (r(2) = 0.31, P < .05), and poly (adenosine diphosphate-ribose) polymerase (r(2) = 0.30, P < .05). These myocardial apoptotic activities also correlated with remodeling strain: cytochrome c (r(2) = 0.02, P < .05), mitochondrial Bax (r(2) = 0.28, P < .05), caspase-3 (r(2) = 0.43, P < .05), and poly (adenosine diphosphate-ribose) polymerase (r(2) = 0.37, P < .05). CONCLUSION: Increase in regional remodeling strain led to an increase in myocardial apoptosis and regional contractile dysfunction in heart failure.