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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Pathol
2014 ; 184
(1
): 171-83
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Histopathological evaluation of the diversity of cells susceptible to H5N1
virulent avian influenza virus
#MMPMID24200852
Ogiwara H
; Yasui F
; Munekata K
; Takagi-Kamiya A
; Munakata T
; Nomura N
; Shibasaki F
; Kuwahara K
; Sakaguchi N
; Sakoda Y
; Kida H
; Kohara M
Am J Pathol
2014[Jan]; 184
(1
): 171-83
PMID24200852
show ga
Patients infected with highly pathogenic avian influenza A H5N1 viruses (H5N1
HPAIV) show diffuse alveolar damage. However, the temporal progression of tissue
damage and repair after viral infection remains poorly defined. Therefore, we
assessed the sequential histopathological characteristics of mouse lung after
intranasal infection with H5N1 HPAIV or H1N1 2009 pandemic influenza virus (H1N1
pdm). We determined the amount and localization of virus in the lung through IHC
staining and in situ hybridization. IHC used antibodies raised against the virus
protein and antibodies specific for macrophages, type II pneumocytes, or
proliferating cell nuclear antigen. In situ hybridization used RNA probes against
both viral RNA and mRNA encoding the nucleoprotein and the hemagglutinin protein.
H5N1 HPAIV infection and replication were observed in multiple lung cell types
and might result in rapid progression of lung injury. Both type II pneumocytes
and macrophages proliferated after H5N1 HPAIV infection. However, the abundant
macrophages failed to block the viral attack, and proliferation of type II
pneumocytes failed to restore the damaged alveoli. In contrast, mice infected
with H1N1 pdm exhibited modest proliferation of type II pneumocytes and
macrophages and slight alveolar damage. These results suggest that the virulence
of H5N1 HPAIV results from the wide range of cell tropism of the virus, excessive
virus replication, and rapid development of diffuse alveolar damage.