Literature DB >> 2548334

Glycoprotein gIII deletion mutants of pseudorabies virus are impaired in virus entry.

T C Mettenleiter1.   

Abstract

gIII is one of the major structural glycoproteins of pseudorabies virus (PrV). Though nonessential for replication in cell culture, it plays a prominent role in virus adsorption and virus release from infected cells. In this study the effect of inactivation of gIII on virus uptake into cells was investigated using isogenic PrV glycoprotein mutants. Kinetic analyses demonstrated that deletion of the gIII gene severely impaired entry of PrV into cells, whereas inactivation of the genes coding for nonessential glycoproteins gI, gp63, or gX had no influence on the rate of virus penetration. Loss of gIII is therefore associated with a reduced rate of virus penetration indicating a gIII-independent way of virus entry which is significantly slower than the gIII-dependent penetration process.

Entities:  

Mesh:

Substances:

Year:  1989        PMID: 2548334     DOI: 10.1016/0042-6822(89)90635-1

Source DB:  PubMed          Journal:  Virology        ISSN: 0042-6822            Impact factor:   3.616


  79 in total

1.  Structure-based functional analyses of domains II and III of pseudorabies virus glycoprotein H.

Authors:  Sebastian W Böhm; Elisa Eckroth; Marija Backovic; Barbara G Klupp; Felix A Rey; Thomas C Mettenleiter; Walter Fuchs
Journal:  J Virol       Date:  2014-11-12       Impact factor: 5.103

2.  Growth, physicochemical properties, and morphogenesis of Chinese wild-type PRV Fa and its gene-deleted mutant strain PRV SA215.

Authors:  Ling Zhu; Yue Yi; Zhiwen Xu; Lu Cheng; Shanhu Tang; Wanzhu Guo
Journal:  Virol J       Date:  2011-06-04       Impact factor: 4.099

3.  Random transposon-mediated mutagenesis of the essential large tegument protein pUL36 of pseudorabies virus.

Authors:  Britta S Möhl; Sindy Böttcher; Harald Granzow; Walter Fuchs; Barbara G Klupp; Thomas C Mettenleiter
Journal:  J Virol       Date:  2010-06-09       Impact factor: 5.103

4.  Generation and Efficacy Evaluation of a Recombinant Pseudorabies Virus Variant Expressing the E2 Protein of Classical Swine Fever Virus in Pigs.

Authors:  Yimin Wang; Jin Yuan; Xin Cong; Hua-Yang Qin; Chun-Hua Wang; Yongfeng Li; Su Li; Yuzi Luo; Yuan Sun; Hua-Ji Qiu
Journal:  Clin Vaccine Immunol       Date:  2015-08-26

5.  Marek's disease virus expresses multiple UL44 (gC) variants through mRNA splicing that are all required for efficient horizontal transmission.

Authors:  Keith W Jarosinski; Nikolaus Osterrieder
Journal:  J Virol       Date:  2012-05-16       Impact factor: 5.103

6.  Mapping of sequences in Pseudorabies virus pUL34 that are required for formation and function of the nuclear egress complex.

Authors:  Lars Paßvogel; Patricia Trübe; Franziska Schuster; Barbara G Klupp; Thomas C Mettenleiter
Journal:  J Virol       Date:  2013-02-06       Impact factor: 5.103

7.  The UL7 gene of pseudorabies virus encodes a nonessential structural protein which is involved in virion formation and egress.

Authors:  Walter Fuchs; Harald Granzow; Robert Klopfleisch; Barbara G Klupp; Daniela Rosenkranz; Thomas C Mettenleiter
Journal:  J Virol       Date:  2005-09       Impact factor: 5.103

8.  Interspecific recombination between two ruminant alphaherpesviruses, bovine herpesviruses 1 and 5.

Authors:  François Meurens; Günther M Keil; Benoît Muylkens; Sacha Gogev; Frédéric Schynts; Sandra Negro; Laetitia Wiggers; Etienne Thiry
Journal:  J Virol       Date:  2004-09       Impact factor: 5.103

9.  Effect of brefeldin A on alphaherpesvirus membrane protein glycosylation and virus egress.

Authors:  M E Whealy; J P Card; R P Meade; A K Robbins; L W Enquist
Journal:  J Virol       Date:  1991-03       Impact factor: 5.103

10.  Pseudorabies virus mutants lacking the essential glycoprotein gII can be complemented by glycoprotein gI of bovine herpesvirus 1.

Authors:  I Rauh; F Weiland; F Fehler; G M Keil; T C Mettenleiter
Journal:  J Virol       Date:  1991-02       Impact factor: 5.103

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.