Early Nuclear Events after Herpesviral Infection.
ATRX
CMV
DAXX
DNA-damage repair
DNA-damage response
HHV-6
HR
HSV-1
Herpes simplex virus
Herpesviruses
ICP-0
IE-1
KSHV
Kaposi’s sarcoma-associated herpesvirus
ND10
NHEJ
ORF75
PML
PML nuclear bodies
SP100
cytomegalovirus
double strand break
double-stranded DNA virus
homology repair
infection
non-homologous end joining
nuclear DNA sensors
restriction factors
virus
virus-host interaction
Journal
Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588
Informations de publication
Date de publication:
07 Sep 2019
07 Sep 2019
Historique:
received:
23
07
2019
revised:
29
08
2019
accepted:
03
09
2019
entrez:
11
9
2019
pubmed:
11
9
2019
medline:
11
9
2019
Statut:
epublish
Résumé
Herpesviruses are important pathogens that can cause significant morbidity and mortality in the human population. Herpesviruses have a double-stranded DNA genome, and viral genome replication takes place inside the nucleus. Upon entering the nucleus, herpesviruses have to overcome the obstacle of cellular proteins in order to enable viral gene expression and genome replication. In this review, we want to highlight cellular proteins that sense incoming viral genomes of the DNA-damage repair (DDR) pathway and of PML-nuclear bodies (PML-NBs) that all can act as antiviral restriction factors within the first hours after the viral genome is released into the nucleus. We show the function and significance of both nuclear DNA sensors, the DDR and PML-NBs, and demonstrate for three human herpesviruses of the alpha-, beta- and gamma-subfamilies, HSV-1, HCMV and KSHV respectively, how viral tegument proteins antagonize these pathways.
Identifiants
pubmed: 31500286
pii: jcm8091408
doi: 10.3390/jcm8091408
pmc: PMC6780142
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Subventions
Organisme : European Union's Framework Program for Research and Innovation Horizon 2020 (2014-2020)
ID : 703896
Organisme : IZKF Erlangen
ID : J57
Organisme : IZKF Erlangen
ID : A66
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