2007
DOI: 10.1128/jvi.00078-07
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Cell-Cell Fusion Induced by Measles Virus Amplifies the Type I Interferon Response

Abstract: Measles virus (MeV) infection is characterized by the formation of multinuclear giant cells (MGC). We report that beta interferon (IFN-␤

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Cited by 45 publications
(34 citation statements)
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“…This implies that membrane fusion is not a limiting factor in this experimental system. Syncytium formation is limited after experimental infection of monkeys (14,26,29), and extensive fusion can be detrimental because it ampli- fies the type I interferon response (18). Thus, wild-type MV may be under selective pressure to limit fusion; from this perspective, the generation of F-protein TM mutants with enhanced fusion function is more likely than if wild-type MV were highly fusogenic.…”
Section: Discussionmentioning
confidence: 99%
“…This implies that membrane fusion is not a limiting factor in this experimental system. Syncytium formation is limited after experimental infection of monkeys (14,26,29), and extensive fusion can be detrimental because it ampli- fies the type I interferon response (18). Thus, wild-type MV may be under selective pressure to limit fusion; from this perspective, the generation of F-protein TM mutants with enhanced fusion function is more likely than if wild-type MV were highly fusogenic.…”
Section: Discussionmentioning
confidence: 99%
“…However, the mechanism by which the virus induces the formation of syncytia has not yet been elucidated. Possibly, fusion may be guided by the GaHV-1 virus through the interaction of envelope glycoproteins with cell membrane receptors, similarly to the infection by measles virus, thereby ensuring their replication and spread (Herschke et al, 2007).…”
Section: Pathological Immunohistochemical and Molecular Findings Inmentioning
confidence: 99%
“…CD209 and TLR2 do not serve as entry receptors but actively trigger (TLR2) or modulate (CD209) signaling pathways in DCs. In addition to their role in entry, CD150 and CD46 may also modulate signaling pathways in DCs attenuated rather than wild-type strains to replicate in DCs (Ohgimoto et al 2007), and the ability of induce formation of multinucleated giant cells in mature, but not immature DCs (and concomitantly, amplification of type I IFN production) was found restricted to a CD46-adapted strain (Herschke et al 2007). This is in contrast to earlier findings where wild-type MV (or recombinants expressing wild-type H protein) preferentially caused fusion in DCs (Ohgimoto et al 2001).…”
Section: Infection and DC Viability And Maturationmentioning
confidence: 95%