Experimental Studies Of Olfactory Epithelium In Mice Infected With Enfluenza Virus

Virus infection in upper respiratory tract as one of main causes of olfactory dysfunction is widely accepted, but the mechanism is still poorly understood. We have performed series studies against apoptosis of olfactory sensory neurons (OSNs) and regeneration of basal cell in olfactory mucosa, and related genes which regulate cell apoptosis. Further more, we put forward that virus infection of upper respiratory tract disturd the balance between apoptosiss of OSNs and regeneration of basal cells, resulting in OSNs losing, might be one of etiopathogenesis of post-virus olfactory dysfunction (PVOD). Objective1. To study the expression of olfactory marker protein (OMP) in the olfactory epithelium of mice post enfluenza infection nasal cavity to elucidate the possible mechanism.2. To study apoptosis of OSNs and regeneration of basal cells in olfactory epithelium of mice infected with enfluenza virus, and find out how the apoptosis related genes, BCL2 and BAX, regulate the pathologic course.3. To determine that nitride oxide (NO) and its rate-limiting enzyme, inducible nitride oxide synthase (iNOS), regulate apotosis of OSNs.