Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-6-19
pubmed:abstractText
Closing the Sendai virus C protein open reading frames (rSeV-DeltaC virus) results in the production of virus particles with highly reduced infectivity. Besides, the Sendai virus C proteins interact with Alix/AIP1 and Alix suppression negatively affects Sendai virus like particle (VLP) budding. Similarly, the Sendai virus M protein has been shown to interact with Alix. On this basis, it has been suggested that Sendai virus budding involves recruitment of the multivesicular body formation machinery. We follow, here, the production of SeV particles upon regular virus infection. We find that neither Alix suppression nor dominant negative-VPS4A expression, applied separately or in combination, affects physical or infectious virion production. This contrasts with the observed decrease of SV5 virion production upon dominant negative-VPS4A expression. Finally, we show that suppression of more than 70% of a GFP/C protein in the background of a rSeV-DeltaC virus infection has no effect either on SeV particle production or on virus particle infectivity. Our results contrast with what has been published before. Possible explanations for this discrepancy are discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
365
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
101-12
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Sendai virus budding in the course of an infection does not require Alix and VPS4A host factors.
pubmed:affiliation
Department of Microbiology and Molecular Medicine, University of Geneva Medical School, CMU, 1 rue Michel Servet, 1211 Geneva 4, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't