scholarly journals Inhibition of Duck Hepatitis B Virus Infection by a Myristoylated Pre-S Peptide of the Large Viral Surface Protein

2002 ◽  
Vol 76 (4) ◽  
pp. 1986-1990 ◽  
Author(s):  
Stephan Urban ◽  
Philippe Gripon

ABSTRACT We have used the duck hepatitis B virus (DHBV) model to study the interference with infection by a myristoylated peptide representing an N-terminal pre-S subdomain of the large viral envelope protein. Although lacking the essential part of the carboxypeptidase D (formerly called gp180) receptor binding site, the peptide binds hepatocytes and subsequently blocks DHBV infection. Since its activity requires an amino acid sequence involved in host discrimination between DHBV and the related heron HBV (T. Ishikawa and D. Ganem, Proc. Natl. Acad. Sci. USA 92:6259-6263, 1995), we suggest that it is related to the postulated host-discriminating cofactor of infection.

2004 ◽  
Vol 78 (4) ◽  
pp. 1873-1881 ◽  
Author(s):  
Jisu Li ◽  
Shuping Tong ◽  
Hong Bock Lee ◽  
Ana Luisa Perdigoto ◽  
Hans Christian Spangenberg ◽  
...  

ABSTRACT Envelope protein precursors of many viruses are processed by a basic endopeptidase to generate two molecules, one for receptor binding and the other for membrane fusion. Such a cleavage event has not been demonstrated for the hepatitis B virus family. Two binding partners for duck hepatitis B virus (DHBV) pre-S envelope protein have been identified. Duck carboxypeptidase D (DCPD) interacts with the full-length pre-S protein and is the DHBV docking receptor, while duck glycine decarboxylase (DGD) has the potential to bind several deletion constructs of the pre-S protein in vitro. Interestingly, DGD but not DCPD expression was diminished following prolonged culture of primary duck hepatocytes (PDH), which impaired productive DHBV infection. Introduction of exogenous DGD promoted formation of protein-free viral genome, suggesting restoration of several early events in viral life cycle. Conversely, blocking DGD expression in fresh PDH by antisense RNA abolished DHBV infection. Moreover, addition of DGD antibodies soon after virus binding reduced endogenous DGD protein levels and impaired production of covalently closed circular DNA, the template for DHBV gene expression and genome replication. Our findings implicate this second pre-S binding protein as a critical cellular factor for productive DHBV infection. We hypothesize that DCPD, a molecule cycling between the cell surface and the trans-Golgi network, targets DHBV particles to the secretary pathway for proteolytic cleavage of viral envelope protein. DGD represents the functional equivalent of other virus receptors in its interaction with processed viral particles.


2006 ◽  
Vol 13 (8) ◽  
pp. 515-522 ◽  
Author(s):  
R. Welschinger ◽  
Y. Cossart ◽  
J. Pouliopoulos ◽  
R. Dixon ◽  
K. Vickery

Virology ◽  
1998 ◽  
Vol 242 (2) ◽  
pp. 266-278 ◽  
Author(s):  
Elena V. Gazina ◽  
Bo Lin ◽  
Andrea Gallina ◽  
Gabriele Milanesi ◽  
David A. Anderson

2007 ◽  
Vol 81 (10) ◽  
pp. 5014-5023 ◽  
Author(s):  
Claudia Maenz ◽  
Shau-Feng Chang ◽  
Alicja Iwanski ◽  
Michael Bruns

ABSTRACT Hepatitis B viruses exhibit a narrow host range specificity that is believed to be mediated by a domain of the large surface protein, designated L. For duck hepatitis B virus, it has been shown that the pre-S domain of L binds to carboxypeptidase D, a cellular receptor present in many species on a wide variety of cell types. Nonetheless, only hepatocytes become infected. It has remained vague which viral features determine host range specificity and organotropicity. By using chymotrypsin to treat duck hepatitis B virus, we addressed the question of whether a putative fusogenic region within the amino-terminal end of the small surface protein may participate in viral entry and possibly constitute one of the determinants of the host range of the virus. Addition of the enzyme to virions resulted in increased infectivity. Remarkably, even remnants of enzyme-treated subviral particles proved to be inhibitory to infection. A noninfectious deletion mutant devoid of the binding region for carboxypeptidase D could be rendered infectious for primary duck hepatocytes by treatment with chymotrypsin. Although because of the protease treatment mutant and wild-type viruses may have become infectious in an unspecific and receptor-independent manner, their host range specificity was not affected, as shown by the inability of the virus to replicate in different hepatoma cell lines, as well as primary chicken hepatocytes. Instead, the organotropicity of the virus could be reduced, which was demonstrated by infection of primary duck kidney cells.


1988 ◽  
Vol 62 (3) ◽  
pp. 861-865 ◽  
Author(s):  
F Imazeki ◽  
K Yaginuma ◽  
M Omata ◽  
K Okuda ◽  
M Kobayashi ◽  
...  

Virology ◽  
1993 ◽  
Vol 192 (1) ◽  
pp. 217-223 ◽  
Author(s):  
Sylvie Chassot ◽  
Véronique Lambert ◽  
Alan Kay ◽  
Catherine Godinot ◽  
Bernard Roux ◽  
...  

Author(s):  
Konrad Oexle ◽  
Hubert E. Blum ◽  
Eike Walter ◽  
Wolf-Bernhard Offensperger ◽  
Silke Offensperger ◽  
...  

1991 ◽  
Vol 106 (3) ◽  
pp. 435-443 ◽  
Author(s):  
S. M. Murray ◽  
J. S. Freiman ◽  
K. Vickery ◽  
D. Lim ◽  
Y. E. Cossart ◽  
...  

SUMMARYThe efficacy of three proprietary glutaraldehyde disinfectants and their component bases was assessed using the duck hepatitis B virus (DHBV) model. Inactivation of infectivity of undiluted serum containing 106·8ID50/ml DHBV was assessed after a mixture with an equal volume of disinfectant had stood at room temperature for 10 min. A dried spill of infectious serum was simulated using sterile filter paper disks, saturated with serum containing DHBV, dried and then exposed to test disinfectant for 10 min. Residual infectivity, and hence the reduction in virus titre, was determined by inoculation of dilutions of the treated samples into 1-day-old ducklings. A greater than 3 log10reduction in virus titre could be demonstrated for the disinfectants as well as for some of their component bases. Disinfectant activity varied according to the method of viral presentation but a reduction of exposure time from 10 to 2·5 min did not diminish activity. The experimental protocol permits a comparative and quantitative assessment of the efficacy of both established and new disinfectants.


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