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 | Differential expression of transforming growth factor�beta1 and HBx enhances hepatitis B virus replication and augments host immune cytokines and chemokines |
Author's Name | Fahad N, Almajhdi, Ahmed Y. Al-Qudari, Zahid Hussain |
Journal Name | Annals of Hepatology |
Pubmed ID | 23619257 |
Abstract | BACKGROUND/AIMS: This study investigated how HBV replication and host immune response are effected by reduced expression of TGF-beta1 and HBx.This study investigated how HBV replication and host immune response are effected by reduced expression of TGF-beta1 and HBx.MATERIAL AND METHODS:Short interfering RNA (siRNA) knockdown technology has been used to examine the role of TGF-beta1 in hepatitis B virus replication. The siTGF-beta1 has been transfected along with 1.3mer HBV x-null to investigate the knockdown effect of TGF-beta1 on HBV replication and host immune factors. RESULTS: In this study, we found that diminished expression of TGF-beta1 and increased expression of HBx enhances HBV replication several folds. The differential expression of TGF-beta1 and HBx also stimulated transcriptional viral replicative intermediate (pgRNA) and secretion of core and e antigen at translational level. Consequently, several cytokines such as IL-2, IL-8 and chemokine monocyte- chemoattractant protein (MCP-1) were increased significantly in response to stimulation of HBV replication. In contrast, TNF-alpha and RANTES mRNA expression increased insignificantly in response to enhanced HBV replication.CONCLUSIONS:We concluded that reduced expression of TGF-beta1 together with HBx expression stimulate HBV replication and immune response, although the underlying mechanism of stimulation most likely differs. |
Used Model | HepG2 cells |
DOI | NA |