Pulmonary pathology in fatal human influenza A (H1N1) infection.
- Author:
Xue-jing DUAN
1
;
Yong LI
;
En-cong GONG
;
Jue WANG
;
Fu-dong LÜ
;
He-qiu ZHANG
;
Lin SUN
;
Zhu-jun YUE
;
Chen-chao SONG
;
Shi-Jie ZHANG
;
Ning LI
;
Jie DAI
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Adult; Aged; Alveolar Epithelial Cells; pathology; Antigens, Viral; metabolism; Apoptosis; Autopsy; Biopsy, Needle; Bronchiolitis, Viral; pathology; Child; Child, Preschool; Female; Hemagglutinin Glycoproteins, Influenza Virus; metabolism; Humans; Influenza A Virus, H1N1 Subtype; immunology; Influenza, Human; metabolism; mortality; pathology; virology; Lung; immunology; metabolism; pathology; Male; Middle Aged; Nuclear Proteins; metabolism; Pulmonary Alveoli; pathology; Pulmonary Fibrosis; pathology; Young Adult
- From: Chinese Journal of Pathology 2011;40(12):825-829
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the pulmonary pathology in patients died of fatal human influenza A(H1N1) infection.
METHODSEight cases of fatal human influenza A (H1N1) infection, including 2 autopsy cases and 6 paramortem needle puncture biopsies, were enrolled into the study. Histologic examination, immunohistochemitry, flow cytometry and Western blotting were carried out.
RESULTSThe major pathologic changes included necrotizing bronchiolitis with surrounding inflammation, diffuse alveolar damage and pulmonary hemorrhage. Influenza viral antigen expression was detected in the lung tissue by Western blotting. Immunohistochemical study demonstrated the presence of nuclear protein and hemagglutinin virus antigens in parts of trachea, bronchial epithelium and glands, alveolar epithelium, macrophages and endothelium. Flow cytometry showed that the apoptotic rate of type II pneumocytes (32.15%, 78.15%) was significantly higher than that of the controls (1.93%, 3.77%).
CONCLUSIONNecrotizing bronchiolitis, diffuse alveolar damage and pulmonary hemorrhage followed by pulmonary fibrosis in late stage are the major pathologic changes in fatal human influenza A (H1N1) infection.
