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Naoya Fujino, Hiroshi Kubo, Chiharu Ota, Takaya Suzuki, Toru Takahashi, Mitsuhiro Yamada, Satoshi Suzuki, Takashi Kondo, Ryouichi Nagatomi, Yukiko Tando, Mutsuo Yamaya, Increased Severity of 2009 Pandemic Influenza A Virus Subtype H1N1 Infection in Alveolar Type II Cells From Patients With Pulmonary Fibrosis, The Journal of Infectious Diseases, Volume 207, Issue 4, 15 February 2013, Pages 692–693, https://doi.org/10.1093/infdis/jis739
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To the Editor—Weinheimer et al [1] reported that influenza A viruses preferentially infect alveolar epithelial type II (ATII) cells in lung tissue explants and suggested that the pathogenicity of influenza A viruses is associated with the ability of these viruses to replicate in ATII cells and induce the production of inflammatory cytokines. In contrast, an epidemiological study by Nguyen-Van-Tam et al [2] demonstrated that chronic pulmonary comorbidities such as pulmonary fibrosis were risk factors for poor outcomes for 2009 pandemic influenza A virus subtype H1N1 (A[H1N1]pdm09) infection. Pulmonary fibrosis is a collective and clinicopathological term for a disease characterized by shortness of breath during exercise, abnormal lung physiology, reduced gas transfer, and excessive scar formation in the lung interstitium. Two studies using genome-wide RNA interference screening identified host factors that are required for the replication of influenza virus [3, 4]. These studies suggest that not only viral strains but also host factors associated with existing pulmonary diseases should be studied to gain a better understanding of the mechanisms of influenza A virus pathogenesis.
