Background/Aim: Influenza A virus (IAV) infection causes an inflammatory response to the respiratory mucosa. The viral glycoprotein hemagglutinin (HA) binds to the sialylated voltage-dependent Ca 2+ channel (Cav1.2) in ciliated epithelium. The binding of HA and sialylated Cav1.2 is considered essential to IAV infection, entry, and IAVinduced Ca 2+ oscillation. The epipharynx comprises the ciliated epithelium, which is the initial target for viruses that cause upper respiratory tract infections. Previously, we showed that epipharyngeal abrasive therapy (EAT), a treatment for chronic epipharyngitis in Japan, which scratches the epipharyngeal mucosa with a cotton swab containing zinc chloride, induces squamous metaplasia. In this study, we evaluated whether squamous metaplasia by EAT affects the expression patterns of Cav1.2. Patients and Methods: The study subjects were seven patients who had not been treated with EAT and 11 patients who had. For the immunohistochemical assessment of the epipharyngeal mucosa, the staining intensity of Cav1.2 was described using the immunohistochemical score (IHC score). Results: The IHC scores for Cav1.2 in the EAT-treated group was 4.19fold lower than those in the non-treated group (p=0.0034).
Conclusion: EAT down-regulates the expression of Cav1.2, a key cell surface molecule in influenza virus entry via squamous metaplasia. Thus, EAT may be a simple method for preventing influenza infection.Influenza A virus (IAV) is an important pathogen that causes annual seasonal epidemics around the world and often leads to unpredictable pandemics (1, 2). Hemagglutinin (HA) is a homotrimer that forms spikes on the viral lipid membrane (3). HAs from human IAVs bind epithelial cell receptors identified as glycans that are terminated by an α2,6-linked sialic acid, but no protein has been identified as a key host cell receptor for IAV so far (4, 5). Recently, it was reported that HA binds to the sialylated voltage-dependent Ca 2+ channel Cav1.2, expressed in the airway epithelium, to 2357