In summary, we report that CS inhibits BAFF in the lung, particularly after long-term exposure; BAFF and S-IgA levels are increased during influenza virus infection; CS exposure prior to influenza virus infection results in reduced BAFF and S-IgA in the lung, decreased Aicda in lung B cells as well as augmented pulmonary inflammation on day 7 after infection; BAFF neutralization results in reduced S-IgA levels and Aicda expression during infection; CSE inhibits virus-mediated BAFF induction in bronchial epithelial cells in vitro, while this inhibition can be prevented by the antioxidant NAC. The gene discussed is CD79A; the disease is infection.