Skip to content
Open access

Clinical characteristics of newborns with the deafness-associated GJB2 variant p.V37I in Changzhi, China

Sep 2026 · Journal of Clinical and Health Sciences · Vol 11 · 0 citations

TL;DR

It is demonstrated that GJB2 variant p.V37I is significantly associated with neonatal hearing loss, underscoring its importance for inclusion in genetic screening programs to facilitate early intervention.

Abstract

Background: Hearing loss affects over 430 million people globally, with genetic factors accounting for at least 50% of congenital cases. The GJB2 gene mutations are the most common cause of non-syndromic hearing impairment (NSHI) worldwide, but the clinical characteristics of c.109G>A (p.V37I) mutation in the GJB2 gene are still indistinct. Objective: To evaluate the prevalence and clinical impact of the c.109G>A (p.V37I) mutation in the GJB2 gene among neonates through audiological and genetic tests. Methods: A cohort of 848 neonates was enrolled between February 2022 and February 2024. All subjects underwent hearing screening and deafness genetic screening for 7 hotspot variants in the GJB2 gene (c.109G>A, c.35delG, c.176_191del16, c.235delC, c.299_300delAT, c.79G>A, and c.341A>G). The association between c.109G>A genotype and hearing phenotype was assessed. Results: The c.109G>A mutation was identified in 24 individuals (2.83%), including 11 heterozygotes, 12 compound heterozygotes, and one homozygote. Audiological test failure rates were significantly higher in c.109G>A carriers compared to non-carriers (18.2% vs. 0.7%, P < 0.001). The homozygous proband exhibited confirmed bilateral hearing loss, and a significant association was observed between genotype and hearing outcomes overall (P = 0.003). Conclusion: This study assessed the prevalence of GJB2 mutations in a Changzhi neonatal cohort. The results demonstrate a significant association between the c.109G>A variant and an increased risk of hearing loss, particularly in homozygous and compound heterozygous carriers. These findings demonstrate that GJB2 variant p.V37I is significantly associated with neonatal hearing loss, underscoring its importance for inclusion in genetic screening programs to facilitate early intervention.

Read PDF

Similar papers

Open access Aug 2026

Two Novel Compound Heterozygous CDH23 Mutations Underlying Non-Syndromic Hearing Loss

Two novel compound heterozygous CDH23 mutations are identified in a thirteen-month-old girl with NSHL, expanding the known spectrum of CDH23 mutation and adding to the understanding of the genotype–phenotype correlations in NSHL.

Pengcheng Xu, Qi Liao, Yun Lin et al. · 0 citations
Review Open access Aug 2026

Founder variant in OTOG causing non-syndromic sensorineural hearing loss in Irish traveller population.

It is demonstrated that protein-truncating variants are scattered throughout the length of the OTOG protein, however, pathogenic missense variants occur only in key domains such as vWD and trypsin inhibitor-like cysteine-rich domains.

Aoife Flynn, Rebecca Finnegan, Aisling Stafford et al. · 0 citations
Case report Open access Jul 2026

Phenotypic Expansion of PPP1R12A-Related Syndrome: A Novel Splicing Variant Associated with Hearing Loss and Inner Ear Malformations

The findings suggest that PPP1R12A-related disorders may exhibit a broader phenotypic variability than previously recognized and it is proposed that HL and inner ear malformations may represent novel features associated with this clinical spectrum.

Giulia Pianigiani, Lara Emily Rosso, A. Morgan et al. · 0 citations
Case report Oct 2026

[Genetic and phenotypic analysis of three children with Neurodevelopmental disorders due to variants of DEAF1 gene].

In vitro functional assay combined with the clinical manifestations of the patients confirmed the pathogenicity of the non-canonical splice site variant in the intronic region, and enriched the mutational spectrum of the DEAF1 gene.

Chao Geng, S. Shangguan, Xiao-Li Chen et al. · 0 citations
Open access Aug 2026

Identification of a Novel homozygous Splice-Site Deletion in KCTD7 Gene Associated with Progressive Myoclonic Epilepsy

The particular phenotype that was observed in the patient is comparable to the ones that are described in the KCTD7 related pathologies, combined with segregation analysis indicating both parents carried the variant heterogeneously present is a strong indication that the identified mutation consists of probably pathoge...

S. Alharazy, Peter Natesan Pushparaj, Rose Jelani et al. · 0 citations

We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.