Herpesvirus is a prevalent pathogen that primarily infects human epithelial cells and has the ability to reside in neurons. In the field of otolaryngology, herpesvirus infection primarily leads to hearing loss and vestibular neuritis and is considered the primary hypothesis regarding the pathogenesis of vestibular neuritis. In this review, we provide a summary of the effects of the herpes virus on cellular processes in both host cells and immune cells, with a focus on HSV-1 as illustrative examples.

Cytomegalovirus infection contributes to 10–30% of congenital hearing loss in children. Vertebrate peripheral auditory organs include the outer, middle, and inner ear. Their development is regulated by multiple signaling pathways. However, most ear diseases due to viral infections are due to congenital infections and reactivation and affect healthy adults to a lesser extent. This may be due to the fact that viral infections affect signaling pathways that are important for the development of peripheral hearing organs. Therefore, an in-depth understanding of the relationship between viral infections and the signaling pathways involved in the development of peripheral hearing organs is important for the prevention and treatment of ear diseases. In this review, we summarize the effects of viruses on signaling pathways and signaling molecules in the development of peripheral auditory organs.

Herpesvirus is a prevalent pathogen that primarily infects human epithelial cells and has the ability to reside in neurons. In the field of otolaryngology, herpesvirus infection primarily leads to hearing loss and vestibular neuritis, and is considered the primary hypothesis regarding the pathogenesis of vestibular neuritis. In this review, we provide a summary of the effects of herpes virus on cellular processes in both host cells and immune cells, with a focus on HSV-1 as illus-trative examples.

Cytomegalovirus infection contributes to 10-30% congenital hearing loss in children. Vertebrate peripheral auditory organs include the outer, middle and inner ear. Their development is regulated by multiple signaling pathways. However, most ear diseases due to viral infections are due to congenital infections and reactivation, and affect healthy adults to a lesser extent. This may be due to the fact that viral infections affect signaling pathways that are important for the development of peripheral hearing organs. Therefore, an in-depth understanding of the relationship between viral infections and the signaling pathways involved in the development of peripheral hearing organs is important for the prevention and treatment of ear diseases. In this review, we summaries the effects of viruses on signaling pathways and signaling molecules in development of peripheral auditory organ, with a focus on Human cytomegalovirus as an example.

The GJB2 gene, which encodes the Connexin26 (Cx26), is the gene most frequently linked to hearing loss. Individuals carrying variants in the GJB2 gene may experience either congenital hearing loss or last-onset progressive hearing loss. The underlying reasons for the variability in hearing remain poorly understood. Current research primarily focuses on conditional knockout mouse models, which generally exhibit moderate to severe hearing loss. To elucidate the mechanisms by which Cx26 variants contribute to mild to moderate hearing loss, this study established a mouse model, the Gjb2D50N/- mice. Auditory brainstem response (ABR) indicated that the Gjb2D50N/- mice led to a mild to moderate increase in hearing thresholds. Further investigations demonstrated that in the Gjb2D50N/- mice, the gap junction plaques (GJPs) between supporting cells were fragmented, and the capacity of outer hair cells (OHCs) to uptake 2-NBDG (a glucose analog) was reduced. In conclusion, we hypothesize that the mild to moderate hearing loss associated with Cx26 variants may not be attributable to structural abnormalities within the cochlea, but rather to dysfunction of GJPs, which compromises the energy supply to OHCs. In this study, we first established a Gjb2 compound heterozygous mouse model that causes mild to moderate hearing loss, for subsequent intervention and treatment.