Nonstructural protein 1 (NS1) is a glycoprotein among the flavivirus genus. It is found in both membrane-associated and soluble secreted forms, has an essential role in viral replication, and modulates the host immune response. NS1 is secreted from infected cells within hours after viral infection, and thus immunodetection of NS1 can be used for early serum diagnosis of dengue fever infections instead of real-time (RT)-PCR. This method is fast, simple, and affordable, and its availability could provide an easy point-of-care testing solution for developing countries. Early studies show that detecting NS1 in cerebrospinal fluid (CSF) samples is possible and can improve the surveillance of patients with dengue-associated neurological diseases. NS1 can be detected postmortem in tissue specimens. It can also be identified using noninvasive methods in urine, saliva, and dried blood spots, extending the availability and effective detection period. Recently, an enzyme-linked immunosorbent assay (ELISA) assay for detecting antibodies directed against Zika virus NS1 has been developed and used for diagnosing Zika infection. This NS1-based assay was significantly more specific than envelope protein-based assays, suggesting that similar assays might be more specific for other flaviviruses as well. This review summarizes the knowledge on flaviviruses’ NS1′s potential role in antigen and antibody diagnosis.

AimThe major clinical manifestations multisystem inflammatory syndrome in children (MIS-C) are fever, gastrointestinal and cardiac. The aim of this study was to describe MIS-C in a series of patients who presented primarily with cervical manifestations.MethodsWe retrospectively reviewed medical records of all patients who met the Centers for Disease Control and Prevention and World Health Organization MIS-C diagnostic criteria treated at Hadassah-Hebrew University Medical Center between April 2020 and September 2021.ResultsOf 37 children diagnosed with MIS-C (median age: 10.2 years, range 1.5-18 years, 20 male) five, 13.5% (median age: 14.4 years, range 9.2-17.5 years) presented with cervical symptoms mimicking neck infections. One was hospitalised with a working diagnosis of retropharyngeal abscess, and four with acute cervical lymphadenitis that did not respond to early antibiotic treatment. All developed full MIS-C phenotype.ConclusionMIS-C may present as cervical inflammation. An ill-appearing child with symptoms and/or signs of cervical inflammation should be evaluated for clinical and laboratory features of MIS-C, thereby facilitating prompt treatment of this potentially fatal disorder.

Background/Objectives: Congenital cytomegalovirus (cCMV) is a leading non-genetic cause of childhood sensorineural hearing loss (SNHL), characterized by heterogeneous and dynamic hearing outcomes. Hearing impairment may be present at birth or emerge later in childhood. This study aimed to characterize hearing trajectories and laterality patterns in children with cCMV, with emphasis on congenital versus delayed-onset SNHL. Methods: We conducted a retrospective study of children with confirmed cCMV who underwent longitudinal audiologic follow-up. Hearing loss was classified as congenital SNHL or delayed-onset SNHL. Better- and poorer-ear thresholds, bilateral involvement, longitudinal changes, and follow-up duration were analyzed. Results: Of 195 included children, 59 (30%) developed SNHL. Congenital SNHL was present in 34 children (17%), while delayed-onset SNHL developed in 25 of 161 children (16%) who were born with normal hearing. Of these delayed-onset cases, 20 (80%) were asymptomatic at birth, while 5 (20%) presented with non-audiological neonatal symptoms. Longitudinal observation of the delayed-onset subgroup revealed that 36 ears developed SNHL during follow-up, spanning infancy through later childhood, including one case identified in early adulthood. Better-ear thresholds were significantly better preserved in delayed-onset SNHL, while poorer-ear thresholds were comparable across groups. Children with SNHL had substantially longer follow-up duration (60 ± 44.5 months) compared with those with normal hearing (37 ± 24.4 months). Conclusions: Children with cCMV-related SNHL exhibit dynamic and asymmetric hearing trajectories with clinically relevant differences between congenital and delayed-onset SNHL. These findings underscore the necessity of a risk-stratified, long-term surveillance framework that ensures individualized long-term monitoring and promotes sustained adherence to follow-up.