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Licensed Unlicensed Requires Authentication Published by De Gruyter January 20, 2015

Sphingolipids in viral infection

  • Jürgen Schneider-Schaulies EMAIL logo and Sibylle Schneider-Schaulies
From the journal Biological Chemistry

Abstract

Viruses exploit membranes and their components such as sphingolipids in all steps of their life cycle including attachment and membrane fusion, intracellular transport, replication, protein sorting and budding. Examples for sphingolipid-dependent virus entry are found for: human immunodeficiency virus (HIV), which besides its protein receptors also interacts with glycosphingolipids (GSLs); rhinovirus, which promotes the formation of ceramide-enriched platforms and endocytosis; or measles virus (MV), which induces the surface expression of its own receptor CD150 via activation of sphingomyelinases (SMases). While SMase activation was implicated in Ebola virus (EBOV) attachment, the virus utilizes the cholesterol transporter Niemann-Pick C protein 1 (NPC1) as ‘intracellular’ entry receptor after uptake into endosomes. Differential activities of SMases also affect the intracellular milieu required for virus replication. Sindbis virus (SINV), for example, replicates better in cells lacking acid SMase (ASMase). Defined lipid compositions of viral assembly and budding sites influence virus release and infectivity, as found for hepatitis C virus (HCV) or HIV. And finally, viruses manipulate cellular signaling and the sphingolipid metabolism to their advantage, as for example influenza A virus (IAV), which activates sphingosine kinase 1 and the transcription factor NF-κB.


Corresponding author: Jürgen Schneider-Schaulies, Institute for Virology and Immunobiology, University of Würzburg, Versbacher Str. 7, D-97078 Würzburg, Germany, e-mail:

Acknowledgments

The authors thank the Deutsche Forschungsgemeinschaft for financial support (Research Unit 2123).

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Received: 2014-11-17
Accepted: 2014-12-12
Published Online: 2015-1-20
Published in Print: 2015-6-1

©2015 by De Gruyter

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