FN Archimer Export Format
PT J
TI Productive Infection of Human Skeletal Muscle Cells by Pandemic and Seasonal Influenza A(H1N1) Viruses
BT 
AF DESDOUITS, Marion
   MUNIER, Sandie
   PREVOST, Marie-Christine
   JEANNIN, Patricia
   BUTLER-BROWNE, Gillian
   OZDEN, Simona
   GESSAIN, Antoine
   VAN DER WERF, Sylvie
   NAFFAKH, Nadia
   CECCALDI, Pierre-Emmanuel
AS 1:1,3,9;2:2,3,8;3:4;4:1,3;5:5,6,7;6:1,3;7:1,3;8:2,3,8;9:2,3;10:1,3,9;
FF 1:;2:;3:;4:;5:;6:;7:;8:;9:;10:;
C1 Inst Pasteur, Unite Epidemiol & Physiopathol Virus Oncogenes, Paris, France.
   Inst Pasteur, Unite Genet Mol Virus ARN, Paris, France.
   CNRS, UMR 3569, Paris, France.
   Inst Pasteur, Paris, France.
   Univ Paris 06, Inst Myol, UM76, Paris, France.
   INSERM, U974, Paris, France.
   CNRS, GH Pitie Salpetriere, UMR7215, Paris, France.
   Univ Paris Diderot, Sorbonne Paris Cite, EA302, Paris, France.
   Univ Paris Diderot, Sorbonne Paris Cite, Paris, France.
C2 INST PASTEUR, FRANCE
   INST PASTEUR, FRANCE
   CNRS, FRANCE
   INST PASTEUR, FRANCE
   UNIV PARIS 06, FRANCE
   INSERM, FRANCE
   CNRS, FRANCE
   UNIV PARIS 07, FRANCE
   UNIV PARIS 07, FRANCE
IN DOAJ
IF 3.534
TC 30
UR https://archimer.ifremer.fr/doc/00344/45492/45034.pdf
LA English
DT Article
AB Besides the classical respiratory and systemic symptoms, unusual complications of influenza A infection in humans involve the skeletal muscles. Numerous cases of acute myopathy and/or rhabdomyolysis have been reported, particularly following the outbreak of pandemic influenza A(H1N1) in 2009. The pathogenesis of these influenza-associated myopathies (IAM) remains unkown, although the direct infection of muscle cells is suspected. Here, we studied the susceptibility of cultured human primary muscle cells to a 2009 pandemic and a 2008 seasonal influenza A(H1N1) isolate. Using cells from different donors, we found that differentiated muscle cells (i. e. myotubes) were highly susceptible to infection by both influenza A(H1N1) isolates, whereas undifferentiated cells (i. e. myoblasts) were partially resistant. The receptors for influenza viruses, alpha 2-6 and alpha 2-3 linked sialic acids, were detected on the surface of myotubes and myoblasts. Time line of viral nucleoprotein (NP) expression and nuclear export showed that the first steps of the viral replication cycle could take place in muscle cells. Infected myotubes and myoblasts exhibited budding virions and nuclear inclusions as observed by transmission electron microscopy and correlative light and electron microscopy. Myotubes, but not myoblasts, yielded infectious virus progeny that could further infect naive muscle cells after proteolytic treatment. Infection led to a cytopathic effect with the lysis of muscle cells, as characterized by the release of lactate dehydrogenase. The secretion of proinflammatory cytokines by muscle cells was not affected following infection. Our results are compatible with the hypothesis of a direct muscle infection causing rhabdomyolysis in IAM patients.
PY 2013
PD NOV
SO Plos One
SN 1932-6203
PU Public Library Science
VL 8
IS 11
UT 000326597400076
DI 10.1371/journal.pone.0079628
ID 45492
ER

EF