Autophagic degradation of lamins facilitates the nuclear egress of herpes simplex virus type 1.
Journal
The Journal of cell biology
ISSN: 1540-8140
Titre abrégé: J Cell Biol
Pays: United States
ID NLM: 0375356
Informations de publication
Date de publication:
04 02 2019
04 02 2019
Historique:
received:
22
01
2018
revised:
02
10
2018
accepted:
08
11
2018
pubmed:
28
12
2018
medline:
18
12
2019
entrez:
28
12
2018
Statut:
ppublish
Résumé
Dendritic cells (DCs) are crucial for the induction of potent antiviral immune responses. In contrast to immature DCs (iDCs), mature DCs (mDCs) are not permissive for infection with herpes simplex virus type 1 (HSV-1). Here, we demonstrate that HSV-1 infection of iDCs and mDCs induces autophagy, which promotes the degradation of lamin A/C, B1, and B2 in iDCs only. This in turn facilitates the nuclear egress of progeny viral capsids and thus the formation of new infectious particles. In contrast, lamin protein levels remain stable in HSV-1-infected mDCs due to an inefficient autophagic flux. Elevated protein levels of KIF1B and KIF2A in mDCs inhibited lamin degradation, likely by hampering autophagosome-lysosome fusion. Therefore, in mDCs, fewer progeny capsids were released from the nuclei into the cytosol, and fewer infectious virions were assembled. We hypothesize that inhibition of autophagic lamin degradation in mDCs represents a very powerful cellular counterstrike to inhibit the production of progeny virus and thus viral spread.
Identifiants
pubmed: 30587512
pii: jcb.201801151
doi: 10.1083/jcb.201801151
pmc: PMC6363456
doi:
Substances chimiques
KIF1B protein, human
0
KIF2A protein, human
0
Lamins
0
Kinesins
EC 3.6.4.4
Banques de données
RefSeq
['NC_001806']
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
508-523Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2019 Turan et al.
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