Persistent autism-relevant behavioral phenotype and social neuropeptide alterations in female mice offspring induced by maternal transfer of PBDE congeners in the commercial mixture DE-71.

Polybrominated diphenyl ethers (PBDEs) are ubiquitous persistent organic pollutants (POPs) that are known neuroendocrine disrupting chemicals with adverse neurodevelopmental effects. PBDEs may act as risk factors for autism spectrum disorders (ASD), characterized by abnormal psychosocial functioning, although direct evidence is currently lacking. Using a translational exposure model, we tested the hypothesis that maternal transfer of a commercial mixture of PBDEs, DE-71, produces ASD-relevant behavioral and neurochemical deficits in female offspring. C57Bl6/N mouse dams (F0) were exposed to DE-71 via oral administration of 0 (VEH/CON), 0.1 (L-DE-71) or 0.4 (H-DE-71) mg/kg bw/d from 3 wk prior to gestation through end of lactation. Mass spectrometry analysis indicated in utero and lactational transfer of PBDEs (in ppb) to F1 female offspring brain tissue at postnatal day (PND) 15 which was reduced by PND 110. Neurobehavioral testing of social novelty preference (SNP) and social recognition memory (SRM) revealed that adult L-DE-71 F1 offspring display deficient short- and long-term SRM, in the absence of reduced sociability, and increased repetitive behavior. These effects were concomitant with reduced olfactory discrimination of social odors. Additionally, L-DE-71 exposure also altered short-term novel object recognition memory but not anxiety or depressive-like behavior. Moreover, F1 L-DE-71 displayed downregulated mRNA transcripts for oxytocin (Oxt) in the bed nucleus of the stria terminalis (BNST) and supraoptic nucleus, and vasopressin (Avp) in the BNST and upregulated Avp1ar in BNST, and Oxtr in the paraventricular nucleus. Our work demonstrates that developmental PBDE exposure produces ASD-relevant neurochemical, olfactory processing and behavioral phenotypes that may result from early neurodevelopmental reprogramming within central social and memory networks.

Longitudinal fecal shedding of SARS-CoV-2, pepper mild mottle virus, and human mitochondrial DNA in COVID-19 patients.

Since the coronavirus disease 2019 (COVID-19) pandemic, wastewater-based epidemiology (WBE) has been widely applied in many countries and regions for monitoring COVID-19 transmission in the population through testing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in wastewater. However, the amount of virus shed by individuals over time based on the stage of infection and accurate number of infections in the community creates challenges in predicting COVID-19 prevalence in the population and interpreting WBE results. In this study, we measured SARS-CoV-2, pepper mild mottle virus (PMMoV), and human mitochondrial DNA (mtDNA) in longitudinal fecal samples collected from 42 COVID-19 patients for up to 42 days after diagnosis. SARS-CoV-2 RNA was detected in 73.1% (19/26) of inpatient study participants in at least one of the collected fecal specimens during the sampling period. Most participants shed the virus within 3 weeks after diagnosis, but five inpatient participants still shed the virus between 20 and 60 days after diagnosis. The median concentration of SARS-CoV-2 in positive fecal samples was 1.08 × 105 genome copies (GC)/gram dry fecal material. PMMoV and mtDNA were detected in 99.4% (154/155) and 100% (155/155) of all fecal samples, respectively. The median concentrations of PMMoV RNA and mtDNA in fecal samples were 1.73 × 107 and 2.49 × 108 GC/dry gram, respectively. These results provide important information about the dynamics of fecal shedding of SARS-CoV-2 and two human fecal indicators in COVID-19 patients. mtDNA showed higher positive rates, higher concentrations, and less variability between and within individuals than PMMoV, suggesting that mtDNA could be a better normalization factor for WBE results than PMMoV.