In:
PLOS Pathogens, Public Library of Science (PLoS), Vol. 17, No. 4 ( 2021-4-19), p. e1009496-
Abstract:
LINE-1 (L1) retrotransposons are autonomous transposable elements that can affect gene expression and genome integrity. Potential consequences of exogenous viral infections for L1 activity have not been studied to date. Here, we report that hepatitis C virus (HCV) infection causes a significant increase of endogenous L1-encoded ORF1 protein (L1ORF1p) levels and translocation of L1ORF1p to HCV assembly sites at lipid droplets. HCV replication interferes with retrotransposition of engineered L1 reporter elements, which correlates with HCV RNA-induced formation of stress granules and can be partially rescued by knockdown of the stress granule protein G3BP1. Upon HCV infection, L1ORF1p localizes to stress granules, associates with HCV core in an RNA-dependent manner and translocates to lipid droplets. While HCV infection has a negative effect on L1 mobilization, L1ORF1p neither restricts nor promotes HCV infection. In summary, our data demonstrate that HCV infection causes an increase of endogenous L1 protein levels and that the observed restriction of retrotransposition of engineered L1 reporter elements is caused by sequestration of L1ORF1p in HCV-induced stress granules.
Type of Medium:
Online Resource
ISSN:
1553-7374
DOI:
10.1371/journal.ppat.1009496
DOI:
10.1371/journal.ppat.1009496.g001
DOI:
10.1371/journal.ppat.1009496.g002
DOI:
10.1371/journal.ppat.1009496.g003
DOI:
10.1371/journal.ppat.1009496.g004
DOI:
10.1371/journal.ppat.1009496.g005
DOI:
10.1371/journal.ppat.1009496.g006
DOI:
10.1371/journal.ppat.1009496.g007
DOI:
10.1371/journal.ppat.1009496.g008
DOI:
10.1371/journal.ppat.1009496.g009
DOI:
10.1371/journal.ppat.1009496.s001
DOI:
10.1371/journal.ppat.1009496.s002
DOI:
10.1371/journal.ppat.1009496.s003
DOI:
10.1371/journal.ppat.1009496.s004
DOI:
10.1371/journal.ppat.1009496.s005
DOI:
10.1371/journal.ppat.1009496.s006
DOI:
10.1371/journal.ppat.1009496.s007
DOI:
10.1371/journal.ppat.1009496.s008
DOI:
10.1371/journal.ppat.1009496.s009
DOI:
10.1371/journal.ppat.1009496.s010
DOI:
10.1371/journal.ppat.1009496.s011
DOI:
10.1371/journal.ppat.1009496.s012
DOI:
10.1371/journal.ppat.1009496.s013
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2021
detail.hit.zdb_id:
2205412-1
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