From the beginning of the coronavirus disease 2019 (COVID-19) pandemic it became evident that children infected with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain mostly asymptomatic or mildly symptomatic. We reviewed the epidemiologic and clinical features of children with SARS-CoV-2 infection. The true prevalence of asymptomatic SARS-CoV-2 infection is most likely underestimated, as asymptomatic children are less frequently tested. Serologic surveys indicate that half of children tested positive for SARS-CoV-2 report no symptoms. Anosmia/ageusia is not frequent in children but it is the strongest predictor of a positive SARS-CoV-2 test. In general, children with COVID-19 are at lower risk of hospitalization and life-threatening complications. Nevertheless, cases of severe disease or a post-infectious multisystem hyperinflammatory syndrome named multisystem inflammatory syndrome in children (MIS-C) have been described. Rarely children with severe COVID-19 develop neurologic complications. In addition, studies indicate that school closures have a limited impact on SARS-CoV-2 transmission, much less than other social distancing measures. The past months new SARS-CoV-2 variants emerged with higher transmissibility and an increased impact on morbidity and deaths. The role of children in the transmission dynamics of these variants must be elucidated. Lastly, preliminary results from COVID-19 vaccine trials indicate very good efficacy and tolerability in children. Very recently the United States Centers for Disease Control and Prevention and other public health authorities recommend vaccination of children 12 years or older to protect them but mostly to contribute to the achievement of herd immunity.

No abstract

Hepatitis C virus (HCV) sequences were detected in cerebrospinal fluid (CSF) in 8 of 13 HCV-positive patients. In four patients harboring different virus strains in serum and peripheral blood mononuclear cells (PBMC), CSF-derived virus was similar to that found in PBMC, which suggests that PBMC could carry HCV into the brain.

WD in children may be obscure and requires extensive investigation to establish the diagnosis. Genetic analysis is needed in equivocal cases.

Glucocerebrosidase gene (GBA) mutations are the most common genetic contributor to Parkinson's disease (PD) and are associated with decreased glucocerebrosidase (GCase) enzymatic activity in PD. PD patients without GBA mutations also exhibit lower levels of GCase activity in the central nervous system suggesting a potential contribution of the enzyme activity in disease pathogenesis, possibly by alteration of lysosomal function. α-synuclein (ASYN), a protein with a central role in PD pathogenesis, has been shown to be secreted partly in association with exosomes. It is possible that a dysfunction of the endocytic pathway through GCase may result in altered exosome release of ASYN. The aim of this study was to examine whether manipulating GCase activity in vivo and in vitro could affect ASYN accumulation and secretion. GCase overexpression in vitro resulted in a significant decrease of exosome secretion. Chronic inhibition of GCase activity in vivo, by administration of the covalent inhibitor conduritol-B epoxide in A53T-synuclein alpha gene Tg mice significantly elevated intracellular oligomeric ASYN species. Importantly, GCase inhibition, induced a profound increase in the number of brain exosomes released, as well as exosome-associated ASYN oligomers. Finally, virus-mediated expression of mutant GBA in the mouse striatum increased ASYN secretion in the same region. Together, these results provide for the first time evidence that a decrease of GCase or overexpression of mutant GCase in a chronic in vivo setting can affect ASYN secretion. Such effects may mediate enhanced propagation of ASYN, driving pathology in GBA-associated PD.