Optimization of Cell Infection Model for Hepatitis Delta Virus (HDV) in hNTCP-overexpressing Hepatoma Cell Lines and Analysis of HDV Genotypes

碩士 === 國立臺灣大學 === 微生物學研究所 === 106 === There are 15-20 million people worldwide chronically coinfected with Hepatitis delta virus (HDV) and Hepatitis B virus (HBV). Simultaneous infection of HBV and HDV may progress easier into the most severe form of hepatitis, fulminant hepatitis, than infection of...

Full description

Bibliographic Details
Main Authors: Yun-Hua Lin, 林昀樺
Other Authors: Pei-Jer Chen
Format: Others
Language:en_US
Published: 2018
Online Access:http://ndltd.ncl.edu.tw/handle/j4q5vp
id ndltd-TW-106NTU05381016
record_format oai_dc
spelling ndltd-TW-106NTU053810162019-05-16T01:00:02Z http://ndltd.ncl.edu.tw/handle/j4q5vp Optimization of Cell Infection Model for Hepatitis Delta Virus (HDV) in hNTCP-overexpressing Hepatoma Cell Lines and Analysis of HDV Genotypes 將D型肝炎病毒的感染模型最佳化並分析不同基因型的表現 Yun-Hua Lin 林昀樺 碩士 國立臺灣大學 微生物學研究所 106 There are 15-20 million people worldwide chronically coinfected with Hepatitis delta virus (HDV) and Hepatitis B virus (HBV). Simultaneous infection of HBV and HDV may progress easier into the most severe form of hepatitis, fulminant hepatitis, than infection of HBV only. Fulminant hepatitis causes rapid death of hepatocytes and liver failure. HDV is a satellite virus of HBV and requires HBV surface proteins (HBs Ag) to serve as viral envelopes. Since HDV is the smallest virus in animal and encodes only one protein, delta antigen, which does not possess the activity to replicate HDV genome, it must utilize host enzymes or other host factors to fulfill its life cycle. To study the role of host factors in HDV life cycle, researchers use primary human hepatocytes (PHH) and HepaRG cells in cell infection model. However, limited supply and difficult management of these cells render experiments hard to be manipulated and reproduced. The discovery of sodium-taurocholate cotransporting polypeptide (NTCP) as a HBV or HDV receptor opens a gate for researchers. Some studies indicate that overexpression of hNTCP makes cells susceptible to HBV or HDV infection. However, HDV infection rate is less than 1% even in hNTCP-overexpressing hepatoma cell line. In order to optimize the infection model in our laboratory, I used suspension infection, treatment of DMSO and PEG8000 and different clones of HDV. In our work, HDV infection rate increases from 0.1% to about 30% in the infection model. I also examine the expression of HDV genotype I, II and IV in the infection model. Since this infection model is established, the relationship between host and HDV can be further examined and eventually, find an effective antiviral therapy. Pei-Jer Chen 陳培哲 2018 學位論文 ; thesis 94 en_US
collection NDLTD
language en_US
format Others
sources NDLTD
description 碩士 === 國立臺灣大學 === 微生物學研究所 === 106 === There are 15-20 million people worldwide chronically coinfected with Hepatitis delta virus (HDV) and Hepatitis B virus (HBV). Simultaneous infection of HBV and HDV may progress easier into the most severe form of hepatitis, fulminant hepatitis, than infection of HBV only. Fulminant hepatitis causes rapid death of hepatocytes and liver failure. HDV is a satellite virus of HBV and requires HBV surface proteins (HBs Ag) to serve as viral envelopes. Since HDV is the smallest virus in animal and encodes only one protein, delta antigen, which does not possess the activity to replicate HDV genome, it must utilize host enzymes or other host factors to fulfill its life cycle. To study the role of host factors in HDV life cycle, researchers use primary human hepatocytes (PHH) and HepaRG cells in cell infection model. However, limited supply and difficult management of these cells render experiments hard to be manipulated and reproduced. The discovery of sodium-taurocholate cotransporting polypeptide (NTCP) as a HBV or HDV receptor opens a gate for researchers. Some studies indicate that overexpression of hNTCP makes cells susceptible to HBV or HDV infection. However, HDV infection rate is less than 1% even in hNTCP-overexpressing hepatoma cell line. In order to optimize the infection model in our laboratory, I used suspension infection, treatment of DMSO and PEG8000 and different clones of HDV. In our work, HDV infection rate increases from 0.1% to about 30% in the infection model. I also examine the expression of HDV genotype I, II and IV in the infection model. Since this infection model is established, the relationship between host and HDV can be further examined and eventually, find an effective antiviral therapy.
author2 Pei-Jer Chen
author_facet Pei-Jer Chen
Yun-Hua Lin
林昀樺
author Yun-Hua Lin
林昀樺
spellingShingle Yun-Hua Lin
林昀樺
Optimization of Cell Infection Model for Hepatitis Delta Virus (HDV) in hNTCP-overexpressing Hepatoma Cell Lines and Analysis of HDV Genotypes
author_sort Yun-Hua Lin
title Optimization of Cell Infection Model for Hepatitis Delta Virus (HDV) in hNTCP-overexpressing Hepatoma Cell Lines and Analysis of HDV Genotypes
title_short Optimization of Cell Infection Model for Hepatitis Delta Virus (HDV) in hNTCP-overexpressing Hepatoma Cell Lines and Analysis of HDV Genotypes
title_full Optimization of Cell Infection Model for Hepatitis Delta Virus (HDV) in hNTCP-overexpressing Hepatoma Cell Lines and Analysis of HDV Genotypes
title_fullStr Optimization of Cell Infection Model for Hepatitis Delta Virus (HDV) in hNTCP-overexpressing Hepatoma Cell Lines and Analysis of HDV Genotypes
title_full_unstemmed Optimization of Cell Infection Model for Hepatitis Delta Virus (HDV) in hNTCP-overexpressing Hepatoma Cell Lines and Analysis of HDV Genotypes
title_sort optimization of cell infection model for hepatitis delta virus (hdv) in hntcp-overexpressing hepatoma cell lines and analysis of hdv genotypes
publishDate 2018
url http://ndltd.ncl.edu.tw/handle/j4q5vp
work_keys_str_mv AT yunhualin optimizationofcellinfectionmodelforhepatitisdeltavirushdvinhntcpoverexpressinghepatomacelllinesandanalysisofhdvgenotypes
AT línyúnhuà optimizationofcellinfectionmodelforhepatitisdeltavirushdvinhntcpoverexpressinghepatomacelllinesandanalysisofhdvgenotypes
AT yunhualin jiāngdxínggānyánbìngdúdegǎnrǎnmóxíngzuìjiāhuàbìngfēnxībùtóngjīyīnxíngdebiǎoxiàn
AT línyúnhuà jiāngdxínggānyánbìngdúdegǎnrǎnmóxíngzuìjiāhuàbìngfēnxībùtóngjīyīnxíngdebiǎoxiàn
_version_ 1719172969656221696