tetano
Editor, Senior Moderator
Clin Pathol. 2014 Nov 6. pii: jclinpath-2014-202441. doi: 10.1136/jclinpath-2014-202441. [Epub ahead of print]
Molecular pathology analyses of two fatal human infections of avian influenza A(H7N9) virus.
Feng Y1, Hu L2, Lu S3, Chen Q3, Zheng Y1, Zeng D1, Zhang J2, Zhang A4, Chen L5, Hu Y6, Zhang Z7.
Author information
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.
Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
KEYWORDS:
H7N9 influenza virus; in situ hybridization; inflammatory response;
PMID:
25378539
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25378539
Molecular pathology analyses of two fatal human infections of avian influenza A(H7N9) virus.
Feng Y1, Hu L2, Lu S3, Chen Q3, Zheng Y1, Zeng D1, Zhang J2, Zhang A4, Chen L5, Hu Y6, Zhang Z7.
Author information
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.
Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
KEYWORDS:
H7N9 influenza virus; in situ hybridization; inflammatory response;
PMID:
25378539
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25378539