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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 J+Virol
2005 ; 79
(23
): 14933-44
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Pathogenicity of influenza viruses with genes from the 1918 pandemic virus:
functional roles of alveolar macrophages and neutrophils in limiting virus
replication and mortality in mice
#MMPMID16282492
Tumpey TM
; García-Sastre A
; Taubenberger JK
; Palese P
; Swayne DE
; Pantin-Jackwood MJ
; Schultz-Cherry S
; Solórzano A
; Van Rooijen N
; Katz JM
; Basler CF
J Virol
2005[Dec]; 79
(23
): 14933-44
PMID16282492
show ga
The Spanish influenza pandemic of 1918 to 1919 swept the globe and resulted in
the deaths of at least 20 million people. The basis of the pulmonary damage and
high lethality caused by the 1918 H1N1 influenza virus remains largely unknown.
Recombinant influenza viruses bearing the 1918 influenza virus hemagglutinin (HA)
and neuraminidase (NA) glycoproteins were rescued in the genetic background of
the human A/Texas/36/91 (H1N1) (1918 HA/NA:Tx/91) virus. Pathogenesis experiments
revealed that the 1918 HA/NA:Tx/91 virus was lethal for BALB/c mice without the
prior adaptation that is usually required for human influenza A H1N1 viruses. The
increased mortality of 1918 HA/NA:Tx/91-infected mice was accompanied by (i)
increased (>200-fold) viral replication, (ii) greater influx of neutrophils into
the lung, (iii) increased numbers of alveolar macrophages (AMs), and (iv)
increased protein expression of cytokines and chemokines in lung tissues compared
with the levels seen for control Tx/91 virus-infected mice. Because pathological
changes in AMs and neutrophil migration correlated with lung inflammation, we
assessed the role of these cells in the pathogenesis associated with 1918
HA/NA:Tx/91 virus infection. Neutrophil and/or AM depletion initiated 3 or 5 days
after infection did not have a significant effect on the disease outcome
following a lethal 1918 HA/NA:Tx/91 virus infection. By contrast, depletion of
these cells before a sublethal infection with 1918 HA/NA:Tx/91 virus resulted in
uncontrolled virus growth and mortality in mice. In addition, neutrophil and/or
AM depletion was associated with decreased expression of cytokines and
chemokines. These results indicate that a human influenza H1N1 virus possessing
the 1918 HA and NA glycoproteins can induce severe lung inflammation consisting
of AMs and neutrophils, which play a role in controlling the replication and
spread of 1918 HA/NA:Tx/91 virus after intranasal infection of mice.