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Molecular pathology analyses of two fatal human infections of avian influenza A(H7N9) virus
  1. Yanling Feng1,
  2. Lvyin Hu2,
  3. Shuihua Lu3,
  4. Qingguo Chen3,
  5. Ye Zheng1,
  6. Dong Zeng1,
  7. Jun Zhang2,
  8. Anli Zhang4,
  9. Liang Chen5,
  10. Yunwen Hu6,
  11. Zhiyong Zhang7
  1. 1Department of Pathology, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
  2. 2Department of Clinical Laboratory, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
  3. 3Department of Respiratory Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
  4. 4Scientific Research Center, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
  5. 5Department of Viral Hepatitis, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
  6. 6Department of Pathogen Diagnosis and Biosafety, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
  7. 7Department of Radiology, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
  1. Correspondence to Dr Yanling Feng, Shanghai Public Health Clinical Center, 2901 Caolang Road, Jinshan, Shanghai 201508, China; fengyanling{at}shaphc.org

Abstract

Aims To investigate the histopathological manifestations of two fatal cases of H7N9 influenza A virus infection.

Methods Pulmonary and hepatic specimens from two fatal cases of H7N9 influenza virus infection were examined using H&E staining. Additionally, in situ hybridisation was performed with probes (ViewRNA) targeting H7N9 RNA and IP-10, interleukin (IL)-6 mRNA. The distribution of surfactant protein A (SP-A), surfactant protein B (SP-B), CD3, CD4, CD8, CD68 and C4d were determined with immunohistochemistry.

Results  Apart from the typical diffuse alveolar damage and hyaline membrane observed in severe influenza infection, we detected H7N9 RNA and massive intrapulmonary production of IP-10 and IL-6 mRNA using in situ hybridisation. Hyperplasia of type II pneumocytes was observed by H&E staining and immunohistochemistry. Proliferating macrophages and clustered neutrophils in the infected lungs were observed, whereas T lymphocytes, especially CD4T helper cells, were markedly depleted. No obvious complement deposition was found in lung tissues.

Conclusions  Our findings suggest that H7N9 influenza virus induced an immunological response towards overt pulmonary inflammation and systemic lymphopenia which led to intense alveolar damage and respiratory failure.

Keywords
  • H7N9 influenza virus
  • in situ hybridization
  • inflammatory response;

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