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Hearing loss is the most common sensory deficit in humans with congenital/prelingual deafness affecting 1 in 1000 children [1]. Delays in treatment for profound sensorineural hearing loss will result in the inability for the patient to develop normal spoken speech and language skills [2]. Additionally, candidacy for cochlear implantation, currently the only medical treatment available for the treatment of profound sensorineural hearing loss, cannot be established without a comprehensive medical examination. Hereditary hearing loss has been acknowledged more than 100 years with nonsyndromic and syndromic form [3]. Nonsyndromic form account for approximately 67% of genetic deafness, whereas a specific syndrome can be identified in about 33% of cases. It is estimated that more than 70 locus may contribute to nonsyndromic deafness. On non-syndromic hereditary hearing loss, there are common list of genes are: GJB2, GJB3, GJA1, MYO6, SLC26A4, SLC26A4, POU3F4, KCNQ4, COCH and 12s4RNA. Single gene, GJB2 (also known as connexin 26) (mutated on chromosome 13q12), is the most common cause of congenital hereditary deafness in many populations [4]. The GJB2 gene encodes connexin 26, a component of gap junctions. Gap junctions are wide expressed in the cochlea and are thought to participate in the recycling of potassium ions from hair cells to the cochlear endolymph. The GJB2 gene contains the instructions for manufacturing a number of proteins, including Connexin 26. Connexin proteins in general are called “gap-junction proteins” which are necessary for cells to communicate with each other. Without sufficient levels of Connexin 26, the potassium flow from hair cells in the cochlea is disrupted, resulting in extremely high levels of potassium in the Corti’s organ, leading to the profound sensorineural hearing loss. Research Article

Mutational Analysis of GJB2 Gene in Non-Syndromic Hearing Loss from Patients at Children’s Hospital 1- Ho Chi Minh City, Vietnam