Correlation of SARS-CoV-2 RNA in wastewater with COVID-19 disease burden in sewersheds.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes the coronavirus disease (COVID-19), is shed in feces and the viral ribonucleic acid (RNA) is detectable in wastewater. A nine-week wastewater epidemiology study of ten wastewater facilities, serving 39% of the state of Utah or 1.26 M individuals was conducted in April and May of 2020. COVID-19 cases were tabulated from within each sewershed boundary. RNA from SARS-CoV-2 was detectable in 61% of 126 wastewater samples. Urban sewersheds serving >100,000 individuals and tourist communities had higher detection frequencies. An outbreak of COVID-19 across two communities positively correlated with an increase in wastewater SARS-CoV-2 RNA, while a decline in COVID-19 cases preceded a decline in RNA. SARS-CoV-2 RNA followed a first order decay rate in wastewater, while 90% of the RNA was present in the liquid phase of the influent. Infiltration and inflow, virus decay and sewershed characteristics should be considered during correlation analysis of SAR-CoV-2 with COVID-19 cases. These results provide evidence of the utility of wastewater epidemiology to assist in public health responses to COVID-19.

A prospective, blinded analysis of A-PROTEIN (recoverin or CAR protein) levels in pediatric patients with central nervous system tumors.

BACKGROUND: Abnormal expression of A-PROTEIN has been identified in a number of tumors including carcinoma of the lung, breast, colon, prostate, and cervix. Brain tumors have been reported to express high plasma levels of A-PROTEIN, suggesting that it may be of significant diagnostic and prognostic value. PROCEDURE: This prospective study evaluated the sensitivity and specificity of A-PROTEIN levels in pediatric brain tumor patients. Patients included those with newly diagnosed disease pre- and post-surgery, during treatment, during routine follow-up, and at recurrence or progression. A total of 154 A-PROTEIN levels from 54 patients were evaluated. RESULTS: For patients without evidence of disease, 42% had normal A-PROTEIN levels, 35% were elevated, and 23% were equivocal. For patients with stable disease, 53% demonstrated normal A-PROTEIN levels, 19% were elevated, and 28% were equivocal. For patients with progressive disease, 53% had normal A-PROTEIN levels, 35% were elevated, and 12% were equivocal. The sensitivity was 35% and the specificity was 50%. A correlation of increased A-PROTEIN levels in patients with increased disease in glial tumors was also identified. CONCLUSIONS: A-PROTEIN levels were not predictive of disease status in children with most brain tumors. However, in patients with glial tumors there was a correlation with increased disease and elevated A-PROTEIN levels. This could represent variability of A-PROTEIN during growth, development, or tumor cell origin and needs further evaluation.