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2015 ; 5
(ä): 17999
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gab.com Text
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Early apoptosis of porcine alveolar macrophages limits avian influenza virus
replication and pro-inflammatory dysregulation
#MMPMID26642934
Chang P
; Kuchipudi SV
; Mellits KH
; Sebastian S
; James J
; Liu J
; Shelton H
; Chang KC
Sci Rep
2015[Dec]; 5
(ä): 17999
PMID26642934
show ga
Pigs are evidently more resistant to avian than swine influenza A viruses,
mediated in part through frontline epithelial cells and alveolar macrophages
(AM). Although porcine AM (PAM) are crucial in influenza virus control, their
mode of control is unclear. To gain insight into the possible role of PAM in the
mediation of avian influenza virus resistance, we compared the host effects and
replication of two avian (H2N3 and H6N1) and three mammalian (swine H1N1, human
H1N1 and pandemic H1N1) influenza viruses in PAM. We found that PAM were readily
susceptible to initial infection with all five avian and mammalian influenza
viruses but only avian viruses caused early and extensive apoptosis (by 6 h of
infection) resulting in reduced virus progeny and moderated pro-inflammation.
Full length viral PB1-F2 present only in avian influenza viruses is a virulence
factor that targets AM for mitochondrial-associated apoptotic cell death. With
the use of reverse genetics on an avian H5N1 virus, we found that full length
PB1-F2 contributed to increased apoptosis and pro-inflammation but not to reduced
virus replication. Taken together, we propose that early apoptosis of PAM limits
the spread of avian influenza viruses and that PB1-F2 could play a contributory
role in the process.
|*Apoptosis
[MESH]
|*Virus Replication
[MESH]
|Animals
[MESH]
|Humans
[MESH]
|Influenza A virus/classification/*physiology
[MESH]