IMPORTANCE Congenital cytomegalovirus (cCMV) infection is a major cause of childhood deafness. Most cCMV infections are not diagnosed without newborn screening, resulting in missed opportunities for directed care.OBJECTIVE To estimate the cost-effectiveness of universal and targeted newborn cCMV screening programs compared with no cCMV screening. DESIGN, SETTING, AND PARTICIPANTS Models were constructed using rates and outcomes from prospective cohort studies of newborn cCMV screening in US postpartum care and early hearing programs. Costs of laboratory testing, treatment, and hearing loss were drawn from Medicaid data and published estimates. The benefits of cCMV screening were assumed to come from antiviral therapy for affected newborns to reduce hearing loss and from earlier identification of hearing loss with postnatal onset. Analyses were performed from July 2014 to March 2016.INTERVENTIONS Models compared universal or targeted cCMV screening of newborns with a failed hearing screen, with standard care for cCMV infection. MAIN OUTCOMES AND MEASURESThe incremental costs of identifying 1 cCMV infection, identifying 1 case of cCMV-related hearing loss, and preventing 1 cochlear implant; the incremental reduction in cases of severe to profound hearing loss; and the differences in costs per infant screened by universal or targeted strategies under different assumptions about the effectiveness of antiviral treatment.

A preliminary set of normative ER data have been generated for a pediatric population between the ages of 5 and 7 yrs, which were significantly different from previously gathered normative adult ER data. In this study, pediatric normative data were warranted for testing children, but ethnic-specific norms were not required to detect middle ear pathology and changes in middle ear status. WBR shows promise as a clinical diagnostic tool for measuring the mechanoacoustic properties of the middle ear and the changes that result in the presence of negative middle ear pressure or MEE.

Key Points• B cells rapidly downregulate CD1d expression after EBV infection, thus abrogating iNKT cell recognition.• EBV-infected B cells induced to express CD1d elicit iNKT cell functions even in the absence of exogenous antigen.Individuals with X-linked lymphoproliferative disease lack invariant natural killer T (iNKT) cells and are exquisitely susceptible to Epstein-Barr virus (EBV) infection. To determine whether iNKT cells recognize or regulate EBV, resting B cells were infected with EBV in the presence or absence of iNKT cells. The depletion of iNKT cells increased both viral titers and the frequency of EBV-infected B cells. However, EBV-infected B cells rapidly lost expression of the iNKT cell receptor ligand CD1d, abrogating iNKT cell recognition. To determine whether induced CD1d expression could restore iNKT recognition in EBVinfected cells, lymphoblastoid cell lines (LCL) were treated with AM580, a synthetic retinoic acid receptor-a agonist that upregulates CD1d expression via the nuclear protein, lymphoid enhancer-binding factor 1 (LEF-1). AM580 significantly reduced LEF-1 association at the CD1d promoter region, induced CD1d expression on LCL, and restored iNKT recognition of LCL. CD1d-expressing LCL elicited interferon g secretion and cytotoxicity by iNKT cells even in the absence of exogenous antigen, suggesting an endogenous iNKT antigen is expressed during EBV infection. These data indicate that iNKT cells may be important for early, innate control of B cell infection by EBV and that downregulation of CD1d may allow EBV to circumvent iNKT cell-mediated immune recognition. (Blood. 2013;122(15):2600-2608