Hayashi Kentaro, Yoshida Hiroshi, Sato Yuko, Tobiume Minoru, Suzuki Yoshio, Ariyoshi Koya, Hasegawa Hideki, Nakajima Noriko
Department of Pathology, National Institute of Infectious Diseases.
Jpn J Infect Dis. 2017 Mar 24;70(2):197-200. doi: 10.7883/yoken.JJID.2016.120. Epub 2016 Jun 30.
We herein report the pulmonary histopathological findings of an autopsy case of post-pandemic season A/H1N1pdm09 infection-associated acute respiratory distress syndrome (ARDS). The lung histology predominantly exhibited findings indicative of the exudative phase of diffuse alveolar damage, with similar inflammation severity observed in all sections. Furthermore, the lung sections only showed a few A/H1N1pdm09 antigen-positive cells along with a low viral RNA copy number. The sequence of the viral hemagglutinin receptor binding site identified a preference for α-2,6 linked sialic acid, suggesting low alveolar epithelial cell infectivity. The pathological findings, in this case, differed in several aspects from those of the first autopsy case of A/H1N1pdm09 infection-associated ARDS in Japan, reported during the 2009 pandemic season. In conclusion, pathological and molecular biological examinations suggested that in the post-pandemic season A/H1N1pdm09 infection, the infection-associated ARDS was not caused by direct infection-induced damage to the alveolar epithelial cells but was rather a result of indirect sepsis-mediated endothelial cell damage.
我们在此报告一例大流行后季节甲型H1N1pdm09感染相关急性呼吸窘迫综合征（ARDS）尸检病例的肺组织病理学发现。肺组织学主要表现为弥漫性肺泡损伤渗出期的特征，所有切片中的炎症严重程度相似。此外，肺切片仅显示少数甲型H1N1pdm09抗原阳性细胞，且病毒RNA拷贝数较低。病毒血凝素受体结合位点的序列显示对α-2,6连接的唾液酸有偏好，提示肺泡上皮细胞感染性较低。该病例的病理发现与2009年大流行季节日本报告的首例甲型H1N1pdm09感染相关ARDS尸检病例在几个方面有所不同。总之，病理和分子生物学检查表明，在大流行后季节甲型H1N1pdm09感染中，感染相关ARDS并非由直接感染导致的肺泡上皮细胞损伤引起，而是间接脓毒症介导的内皮细胞损伤的结果。
