About: Acid ceramidase of macrophages traps herpes simplex virus in multivesicular bodies and protects from severe disease

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Acid ceramidase of macrophages traps herpes simplex virus in multivesicular bodies and protects from severe disease
Creator	Bauer, Michael Edwards, Michael Sodeik, Beate Krawczyk, Adalbert Hardt, Cornelia Duhan, Vikas Greber, Urs Göthert, Joachim Lang, Karl Lang, Philipp Babiychuk, Eduard Bhat, Hilal Bohn, Patrick Burchert, Andreas Cansiz, Feyza Fink, Julian Friebus-Kardash, Justa Friedrich, Sarah-Kim Gulbins, Erich Huber, Magdalena Jastrow, Holger Kleuser, Burkhard Köhrer, Karl Lang, Judith Olszewski, Dominik Probst, Hans Ramos-Nascimento, Ana Schumacher, Fabian Seibel, Jürgen Walkenfort, Bernd Becker, Katrin, Anne
Source	PMC
abstract	Macrophages have important protective functions during infection with herpes simplex virus type 1 (HSV-1). However, molecular mechanisms that restrict viral propagation and protect from severe disease are unclear. Here we show that macrophages take up HSV-1 via endocytosis and transport the virions into multivesicular bodies (MVBs). In MVBs, acid ceramidase (aCDase) converts ceramide into sphingosine and increases the formation of sphingosine-rich intraluminal vesicles (ILVs). Once HSV-1 particles reach MVBs, sphingosine-rich ILVs bind to HSV-1 particles, which restricts fusion with the limiting endosomal membrane and prevents cellular infection. Lack of aCDase in macrophage cultures or in Asah1(−/−) mice results in replication of HSV-1 and Asah1(−/−) mice die soon after systemic or intravaginal inoculation. The treatment of macrophages with sphingosine enhancing compounds blocks HSV-1 propagation, suggesting a therapeutic potential of this pathway. In conclusion, aCDase loads ILVs with sphingosine, which prevents HSV-1 capsids from penetrating into the cytosol.
has issue date	2020-03-12(xsd:dateTime)
bibo:doi	10.1038/s41467-020-15072-8
bibo:pmid	32165633
has license	cc-by
sha1sum (hex)	cb1b098e091c3d41279e8cf754f901388cde8b86
schema:url	https://doi.org/10.1038/s41467-020-15072-8
resource representing a document's title	Acid ceramidase of macrophages traps herpes simplex virus in multivesicular bodies and protects from severe disease
has PubMed Central identifier	PMC7067866
has PubMed identifier	32165633
schema:publication	Nat Commun
resource representing a document's body	covid:cb1b098e091c3d41279e8cf754f901388cde8b86#body_text
is schema:about of	named entity 'enhancing' named entity 'Asah1' named entity 'sphingosine' named entity 'multivesicular bodies' named entity 'fusion' named entity 'HSV-1' named entity 'CERAMIDE' named entity 'ENDOSOMAL MEMBRANE' named entity 'HSV-1' named entity 'PATHWAY' named entity 'CULTURES' named entity 'IMPORTANT' named entity 'INTRALUMINAL' named entity 'RICH' named entity 'UNCLEAR' named entity 'THERAPEUTIC' named entity 'SYSTEMIC' named entity 'ASAH1' named entity 'SPHINGOSINE' named entity 'SOON AFTER' named entity 'REPLICATION' named entity 'MECHANISMS' named entity 'LIMITING' named entity 'PENETRATING' named entity 'CELLULAR' named entity 'VIRAL' named entity 'POTENTIAL' named entity 'BLOCKS' named entity 'MOLECULAR' named entity 'PREVENTS' named entity 'HERPES SIMPLEX VIRUS TYPE 1' named entity 'MULTIVESICULAR BODIES' named entity 'REACH' named entity 'ENDOCYTOSIS' named entity 'CONCLUSION' named entity 'FUNCTIONS' named entity 'MACROPHAGES' named entity 'VESICLES' named entity 'TREATMENT' covid:arg/cb1b098e091c3d41279e8cf754f901388cde8b86 named entity 'FUSION' named entity 'LACK' named entity 'CLUSTER' named entity 'DIE' named entity 'HERE' named entity 'PROPAGATION' named entity 'RESULTS' named entity 'BIND' named entity 'INFECTION' named entity 'PARTICLES'

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