tetano
Editor, Senior Moderator
Virology. 2014 Jul 3;462-463C:241-253. doi: 10.1016/j.virol.2014.05.028. [Epub ahead of print]
Caveolin-1 limits human influenza A virus (H1N1) propagation in mouse embryo-derived fibroblasts.
Bohm K1, Sun L2, Thakor D3, Wirth M4.
Author information
Abstract
Caveolin expression supports the multiplication of retro-, ortho- and paramyxoviruses in susceptible cells. However, human influenza A virus (IAV), an orthomyxovirus, does not multiply efficiently in mouse embryo fibroblasts (MEFs), which are abundant in caveolin-1 (Cav-1). Surprisingly, the absence of Cav-1 in a MEF cell line removed the block for IAV replication and raised the infectious titer 250-fold, whereas the re-introduction of Cav-1 reversed the effect. The monitoring of cellular pathways revealed that Cav-1 loss considerably increased activities of p53. Furthermore, infection of MEF Cav-1 (-/-) induced reactive oxygen species (ROS) and pronounced apoptosis in the late phase of viral multiplication, but no type I IFN response. Strikingly, pharmacological inactivation showed that the elevated levels of ROS together with apoptosis caused the increase of virus yield. Thus, Cav-1 represents a new negative regulator of IAV infection in MEF that diminishes IAV infectious titer by controlling virus-supportive pathways.
Copyright ? 2014 Elsevier Inc. All rights reserved.
KEYWORDS:
Apoptosis; Caveolin-1-deficiency; Human influenza A virus; Mouse embryo-derived fibroblasts; Reactive oxygen species; Reporter gene array; Restriction
PMID:
24999049
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24999049
Caveolin-1 limits human influenza A virus (H1N1) propagation in mouse embryo-derived fibroblasts.
Bohm K1, Sun L2, Thakor D3, Wirth M4.
Author information
Abstract
Caveolin expression supports the multiplication of retro-, ortho- and paramyxoviruses in susceptible cells. However, human influenza A virus (IAV), an orthomyxovirus, does not multiply efficiently in mouse embryo fibroblasts (MEFs), which are abundant in caveolin-1 (Cav-1). Surprisingly, the absence of Cav-1 in a MEF cell line removed the block for IAV replication and raised the infectious titer 250-fold, whereas the re-introduction of Cav-1 reversed the effect. The monitoring of cellular pathways revealed that Cav-1 loss considerably increased activities of p53. Furthermore, infection of MEF Cav-1 (-/-) induced reactive oxygen species (ROS) and pronounced apoptosis in the late phase of viral multiplication, but no type I IFN response. Strikingly, pharmacological inactivation showed that the elevated levels of ROS together with apoptosis caused the increase of virus yield. Thus, Cav-1 represents a new negative regulator of IAV infection in MEF that diminishes IAV infectious titer by controlling virus-supportive pathways.
Copyright ? 2014 Elsevier Inc. All rights reserved.
KEYWORDS:
Apoptosis; Caveolin-1-deficiency; Human influenza A virus; Mouse embryo-derived fibroblasts; Reactive oxygen species; Reporter gene array; Restriction
PMID:
24999049
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24999049