Excessive virus replication, multi-organ failure, and hyperimmune activation have been detected in humans and laboratory animals infected with HPAI H5N1 and with recreated 1918 pandemic influenza virus [47, 48, 49, 50, 51] . The mechanisms responsible for deterioration of lung function and the loss of capacity for lung repair after influenza virus infection are not well understood. Although influenza virus primarily replicates in lung, virus has been detected in extra pulmonary tissues including bone marrow [52, 53] . Our in vitro findings show that progenitor epithelial cells in bone marrow are permissive to influenza virus suggesting that in the event of influenza virus infection, bone marrow progenitor cells may not be available to home to the injured lung to participate in tissue repair. Additional experiments are needed to confirm the infection of progenitor epithelial cells in vivo and to delineate further their roles in local and lung repair following infection with influenza virus.