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Global host immune response: pathogenesis and transcriptional profiling of type A
influenza viruses expressing the hemagglutinin and neuraminidase genes from the
1918 pandemic virus
#MMPMID15308742
Kash JC
; Basler CF
; García-Sastre A
; Carter V
; Billharz R
; Swayne DE
; Przygodzki RM
; Taubenberger JK
; Katze MG
; Tumpey TM
J Virol
2004[Sep]; 78
(17
): 9499-511
PMID15308742
show ga
To understand more fully the molecular events associated with highly virulent or
attenuated influenza virus infections, we have studied the effects of expression
of the 1918 hemagglutinin (HA) and neuraminidase (NA) genes during viral
infection in mice under biosafety level 3 (agricultural) conditions. Using
histopathology and cDNA microarrays, we examined the consequences of expression
of the HA and NA genes of the 1918 pandemic virus in a recombinant influenza
A/WSN/33 virus compared to parental A/WSN/33 virus and to an attenuated virus
expressing the HA and NA genes from A/New Caledonia/20/99. The 1918 HA/NA:WSN and
WSN recombinant viruses were highly lethal for mice and displayed severe lung
pathology in comparison to the nonlethal New Caledonia HA/NA:WSN recombinant
virus. Expression microarray analysis performed on lung tissues isolated from the
infected animals showed activation of many genes involved in the inflammatory
response, including cytokine, apoptosis, and lymphocyte genes that were common to
all three infection groups. However, consistent with the histopathology studies,
the WSN and 1918 HA/NA:WSN recombinant viruses showed increased up-regulation of
genes associated with activated T cells and macrophages, as well as genes
involved in apoptosis, tissue injury, and oxidative damage that were not observed
in the New Caledonia HA/NA:WSN recombinant virus-infected mice. These studies
document clear differences in gene expression profiles that were correlated with
pulmonary disease pathology induced by virulent and attenuated influenza virus
infections.
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