scholarly journals Complementation of recombinant baculoviruses by coinfection with wild-type virus facilitates production in insect larvae of antigenic proteins of hepatitis B virus and influenza virus.

1989 ◽  
Vol 86 (5) ◽  
pp. 1453-1456 ◽  
Author(s):  
P. M. Price ◽  
C. F. Reichelderfer ◽  
B. E. Johansson ◽  
E. D. Kilbourne ◽  
G. Acs
Keyword(s):  
Influenza Virus ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Recombinant Baculoviruses ◽  
Wild Type Virus ◽  
Type Virus ◽  
Wild Type ◽  
Insect Larvae ◽  
Antigenic Proteins ◽  
B Virus

scholarly journals Presence of Replicating Virus in Recombinant Hepadnavirus Stocks Results from Recombination and Can Be Eliminated by the Use of a Packaging Cell Line

2003 ◽  
Vol 77 (5) ◽  
pp. 2873-2881 ◽  
Author(s):  
Uta Klöcker ◽  
Heike Oberwinkler ◽  
Timo Kürschner ◽  
Ulrike Protzer
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Wild Type Virus ◽  
Recombinant Hepatitis ◽  
Type Virus ◽  
Wild Type ◽  
Viral Genomes ◽  
B Virus ◽  
Viral Sequences

ABSTRACT Mutant hepatitis B viruses are useful tools to study the viral life cycle and viral pathogenesis. Furthermore, recombinant hepatitis B viruses are candidate vectors for liver-directed gene therapy. Because wild-type viruses present in recombinant or mutant virus stocks may falsify experimental results and are detrimental for a viral vector, we investigated whether and to what extent wild-type virus is present in recombinant virus stocks and where it originates from. We took advantage of the duck model of hepatitis B virus infection which allows very sensitive detection of replication-competent viruses by infection of primary duck hepatocytes or of ducklings in vivo. Recombinant hepatitis B virus stocks contained significant amounts of wild-type viruses, which were most probably generated by homologous recombination between plasmids containing homologous viral sequences. In addition, replication-competent viral genomes were reconstituted from plasmids which contained replication-deficient but redundant viral sequences. Using a stable cell line for packaging of deficient viral genomes, no wild-type virus was detected, neither by infection of primary hepatocytes nor in vivo.

A novel hepatitis B virus mutant coexisting with wild type virus in a carrier with negative HBsAg yet positive HBeAg and anti-HBs

2009 ◽  
Vol 46 (4) ◽  
pp. 363-366 ◽  
Author(s):  
Yi-Hua Zhou ◽  
Jianxin Zhou ◽  
Lei Li ◽  
Yongchun Bi ◽  
Yong Liu ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Wild Type Virus ◽  
Type Virus ◽  
Wild Type ◽  
B Virus ◽  
Virus Mutant ◽  
Positive Hbeag

scholarly journals Enrichment of a Precore-Minus Mutant of Duck Hepatitis B Virus in Experimental Mixed Infections

1999 ◽  
Vol 73 (5) ◽  
pp. 3616-3622 ◽  
Author(s):  
Yong-Yuan Zhang ◽  
Jesse Summers
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Mutant Virus ◽  
Wild Type Virus ◽  
Type Virus ◽  
Wild Type ◽  
Duck Hepatitis B Virus ◽  
Duck Hepatitis ◽  
B Virus ◽  
Precore Mutant

ABSTRACT A precore-deficient mutant of duck hepatitis B virus (DHBV) produced by site-directed mutagenesis was tested for its ability to compete with wild-type virus in a mixed infection of 3-day-old ducklings. The mutation was shown to produce a cis-acting defect, resulting in a replication rate that was about one-half that of wild-type virus. Accordingly, wild-type virus was rapidly selected during the spread of infection. During the chronic phase of the infection, however, two selection patterns were seen. In 4 of 10 ducks, the wild-type virus slowly replaced the precore mutant. In another four ducks, the precore mutant virus slowly replaced the wild-type virus. In the remaining two ducklings, ratios of wild-type and precore mutant virus fluctuated, with wild-type virus slowly predominating. The replacement of wild-type virus was not due to the emergence of a rapidly replicating variant of the precore mutant, since genomes cloned from the infected ducks retained their original replication defect. Replacement of wild-type virus, however, correlated with elevated anti-core antibody titers, which continued to increase with time. The selection of a precore-negative strain of DHBV may be analogous to the selection for precore mutants of HBV during chronic hepatitis in humans.

scholarly journals Interferon gene transfer by a hepatitis B virus vector efficiently suppresses wild-type virus infection

1999 ◽  
Vol 96 (19) ◽  
pp. 10818-10823 ◽  
Author(s):  
U. Protzer ◽  
M. Nassal ◽  
P.-W. Chiang ◽  
M. Kirschfink ◽  
H. Schaller
Keyword(s):  
Hepatitis B Virus ◽  
Gene Transfer ◽  
Virus Infection ◽  
Hepatitis B ◽  
Virus Vector ◽  
Wild Type Virus ◽  
Type Virus ◽  
Wild Type ◽  
B Virus ◽  
Interferon Gene

scholarly journals Substitution of proline 306 in the reverse transcriptase domain of hepatitis B virus regulates replication

2005 ◽  
Vol 86 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Xu Lin ◽  
Zhang-Mei Ma ◽  
Xin Yao ◽  
Li-Fang He ◽  
Zheng-Hong Yuan ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Reverse Transcriptase ◽  
Wild Type Virus ◽  
Wild Type ◽  
Functional Changes ◽  
Hbv Replication ◽  
B Virus ◽  
Dna Template ◽  
The Impact

The proline residue at position 306 in hepatitis B virus (HBV) reverse transcriptase (rtP306) has been suggested to constrain the conformation of the α-helices in the thumb subdomain that interacts with the viral DNA template-primer. To study the impact of residue rt306 in HBV replication further, 11 site-directed mutants were constructed that substituted rtP306 with different amino acids. The replicative competencies of these mutants were assayed by HepG2 cell transfection and real-time PCR. When rtP306 was substituted with glycine or threonine, the replication competency of these mutants was drastically reduced to 1·96 and 4·51 % of the wild-type HBV level, respectively. When rtP306 was substituted with glutamic acid, the replicative competency of the mutant increased up to 9·4-fold compared with wild-type virus. The results also showed that changes in the replicative competency of these constructed mutants were not associated with functional changes of HBV enhancer I. These results indicate the importance of amino acid(s) at the interface between the thumb and palm subdomains in modulating the replicative competency of HBV isolates. This regulatory residue(s) could serve as a new target for the development of anti-HBV drugs.

Precore/Core Promoter Mutant Hepatitis B Virus Produces More Severe Histologic Liver Disease than Wild Type Hepatitis B Virus

2007 ◽  
Vol 1 (1) ◽  
pp. 41-46 ◽  
Author(s):  
Mamun-Al-Mahtab ◽  
Salimur Rahman ◽  
Mobin Khan ◽  
Ayub Mamun ◽  
Kamal
Keyword(s):  
Liver Disease ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Core Promoter ◽  
Wild Type ◽  
B Virus ◽  
Promoter Mutant
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