Virology: Current Research

Anti-viral and Anti-inflammatory Effects of Camostat and Nafamostat on Influenza Virus and Coronavirus Infections in Human Airway Cells and the Mouse Lungs

Abstract

Mutsuo Yamaya* and Hidekazu Nishimura

Influenza viruses and coronaviruses cause several human diseases, such as bronchitis, bronchiolitis, and pneumonia, and exacerbate bronchial asthma, chronic obstructive pulmonary disease and pulmonary fibrosis. Human airway epithelial cells infected with these viruses release progeny viruses and inflammatory cytokines, such as Interleukin (IL)-1β, IL-6, IL-8 and tumor necrosis factor-α, partly through the activation of nuclear factor kappa B. Modulation of airway damage and inflammation may modulate viral infection-induced airway and lung diseases. Human tracheal and nasal epithelial cells express proteases, including Transmembrane Protease Serine S1 Member 2 (TMPRSS2), and the proteases activate influenza viruses and coronaviruses and the subsequent replication processes of these viruses. The protease inhibitors camostat and nafamostat reduced influenza virus and coronavirus replication and the amounts of cytokines released from human airway epithelial cells. Nafamostat also reduced the release of influenza virus in the lungs of mice. The development of clinically available protease inhibitors is required to treat patients infected with influenza virus or coronavirus.