Baculovirus as a highly efficient gene delivery vector for the expression of hepatitis delta virus antigens in mammalian cells

2005 ◽  
Vol 89 (4) ◽  
pp. 464-473 ◽  
Author(s):  
Kuei-Chun Wang ◽  
Jaw-Chin Wu ◽  
Yao-Chi Chung ◽  
Yi-Chen Ho ◽  
Margaret Dah-Tsyr Chang ◽  
...  
2015 ◽  
Vol 23 (8) ◽  
pp. 726-733 ◽  
Author(s):  
Nan Young Ahn ◽  
Tae-Hun Kim ◽  
Su Jeong Song ◽  
Jeong-Mi Moon ◽  
Tai Hwan Ha ◽  
...  

2007 ◽  
Vol 22 (6) ◽  
pp. 527-544 ◽  
Author(s):  
Hui Zhong ◽  
Zhi-Guo He ◽  
Zheng Li ◽  
Gui-Yuan Li ◽  
Shou-Rong Shen ◽  
...  

2007 ◽  
Vol 1 (1) ◽  
pp. 34-40
Author(s):  
Ying-Wei Chiang ◽  
Jaw-Chin Wu ◽  
Kuei-Chun Wang ◽  
Szu-Ting Chou ◽  
Yu-Chen Hu

Hepatitis delta virus (HDV) is a defective virus that requires the supply of hepatitis B virus surface antigen (HBsAg) for replication and transmission. We have previously demonstrated that co-transduction of BHK cells with Bac- GD, a recombinant baculovirus expressing large hepatitis delta antigen (L-HDAg), and Bac-GS2, another recombinant baculovirus expressing HBsAg, gives rise to the assembly and secretion of 22 nm HBsAg subviral particles and 35-37 nm HDV-like particles (HDV VLP). In this study we uncovered oversize particles (>50 nm in diameter) comprised of HBsAg and L-HDAg and the particle properties varied with the relative dosages of Bac-GD and Bac-GS2, as demonstrated by Western blot, transmission electron microscopy and immunogold labeling. At a given Bac-GS2 dosage, decreasing the Bac-GD dosage resulted in the expression of more HBsAg, elevated secretion of HBsAg subviral particles, incorporation of more HBsAg into the HDV VLP, narrower particle size distribution and lower particle density. These data collectively demonstrated that the composition, and hence the properties, of HDV VLPs could be manipulated by altering the relative expression levels of structure proteins.


2001 ◽  
Vol 75 (16) ◽  
pp. 7489-7493 ◽  
Author(s):  
Yu-Tsueng Liu ◽  
Rob Brazas ◽  
Don Ganem

ABSTRACT Hepatitis delta virus (HDV) is a highly pathogenic human RNA virus whose genome is structurally related to those of plant viroids. Although its spread from cell to cell requires helper functions supplied by hepatitis B virus (HBV), intracellular HDV RNA replication can proceed in the absence of HBV proteins. As HDV encodes no RNA-dependent RNA polymerase, the identity of the (presumably cellular) enzyme responsible for this reaction remains unknown. Here we show that, in contrast to mammalian cells, avian cells do not support efficient HDV RNA replication and that this defect cannot be rescued by provision of HDV gene products in trans. Contrary to earlier assertions, this defect is not due to enhanced apoptosis triggered in avian cells by HDV. Fusion of avian cells to mammalian cells rescues HDV replication in avian nuclei, indicating that the nonpermissive phenotype of avian cells is not due to the presence of dominantly acting inhibitors of replication. Rather, avian cells lack one or more essential permissive factors present in mammalian cells. These results set the stage for the identification of such factors and also explain the failure of earlier efforts to transmit HDV infection to avian hosts harboring indigenous hepadnaviruses.


2013 ◽  
Vol 24 (9) ◽  
pp. 1612-1623 ◽  
Author(s):  
Abirami Lakshminarayanan ◽  
Vijay Kumar Ravi ◽  
Ranjitha Tatineni ◽  
Y. B. R. D. Rajesh ◽  
Vishal Maingi ◽  
...  

2018 ◽  
Vol 53 ◽  
pp. 23-28 ◽  
Author(s):  
Chatwalee Boonthum ◽  
Katawut Namdee ◽  
Mattaka Khongkow ◽  
Sasithont Temisak ◽  
Kaywalee Chatdarong ◽  
...  

Vaccine ◽  
2001 ◽  
Vol 20 (1-2) ◽  
pp. 170-180 ◽  
Author(s):  
Christian Mauch ◽  
Christian Grimm ◽  
Stefan Meckel ◽  
Jack R. Wands ◽  
Hubert E. Blum ◽  
...  

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