Virus Name | Hepatitis B virus |
Virus Short Name | HBV |
Order | Unassigned |
Virus Family | Hepadnaviridae |
Virus Subfamily | N.A. |
Genus | Orthohepadnavirus |
Species | Hepatitis B virus |
Host | Human, mammals |
Cell Tropism | Hepatocytes |
Associated Disease | Hepatitis, hepatocellular carcinoma(chronic infections), cirrhosis |
Mode of Transmission | Sexual contact, blood, maternal-neonatal |
VIPR DB link | N.A. |
ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/reverse-transcribing-dna-and-rna-viruses-2011/w/rt_viruses/155/hepadnaviridae |
Virus Host DB link | N.A. |
Paper Title | DDX3 DEAD-box RNA helicase is a host factor that restricts hepatitis B virus replication at the transcriptional level |
Author's Name | Chunkyu Ko, Sooyoung Lee, Marc P. Windisch, Wang-Shick Ryu |
Journal Name | Journal Of Virology |
Pubmed ID | 25231298 |
Abstract | DDX3 is a member of the DEAD-box RNA helicase family, involved in mRNA metabolism, including transcription, splicing, and translation. We previously identified DDX3 as a hepatitis B virus (HBV) polymerase (Pol) binding protein, and by using a transient transfection, we found that DDX3 inhibits HBV replication at the posttranscriptional level, perhaps following encapsidation. To determine the exact mechanism of the inhibition, we here employed a diverse HBV experimental system. Inconsistently, we found that DDX3-mediated inhibition occurs at the level of transcription. By using tetracycline-inducible HBV-producing cells, we observed that lentivirus-mediated DDX3 expression led to a reduced level of HBV RNAs. Importantly, knockdown of DDX3 by short hairpin RNA resulted in augmentation of HBV RNAs in two distinct HBV replication systems: (i) tetracycline-inducible HBV-producing cells and (ii) constitutive HBV-producing HepG2.2.15 cells. Moreover, DDX3 knockdown in HBV-susceptible HepG2-NTCP cells, where covalently closed circular DNA (cccDNA) serves as the template for viral transcription, resulted in increased HBV RNAs, validating that transcription regulation by DDX3 occurs on a physiological template. Overall, our results demonstrate that DDX3 represents an intrinsic host antiviral factor that restricts HBV transcription. |
Used Model | HepG2 cells |
DOI | 10.1128/JVI.02035-14 |