The pathogenesis of wild type and drug resistant mutant strains of bovine herpesvirus-1 (BHV-1) in the natural host

1993 ◽  
Vol 128 (1-2) ◽  
pp. 43-54 ◽  
Author(s):  
S. E. Gilliam ◽  
A. M. Thackray ◽  
G. A. Brown ◽  
H. J. Field
Keyword(s):  
Bovine Herpesvirus ◽  
Resistant Mutant ◽  
Natural Host ◽  
Drug Resistant ◽  
Wild Type ◽  
Bovine Herpesvirus 1 ◽  
Mutant Strains ◽  
Drug Resistant Mutant ◽  
Herpesvirus 1

EvaGreen-based Multiplex Real-time PCR Assay for Rapid Differentiation of Wild-Type and Glycoprotein E-Deleted Bovine Herpesvirus-1 Strains

2017 ◽  
Vol 28 (4) ◽  
pp. 248-252 ◽  
Author(s):  
Sachin S. Pawar ◽  
Chetan D. Meshram ◽  
Niraj K. Singh ◽  
Mohini Saini ◽  
B. P. Mishra ◽  
...  
Keyword(s):  
Real Time ◽  
Real Time Pcr ◽  
Bovine Herpesvirus ◽  
Wild Type ◽  
Pcr Assay ◽  
Bovine Herpesvirus 1 ◽  
Glycoprotein E ◽  
Herpesvirus 1

scholarly journals Pseudorabies Virus Expressing Bovine Herpesvirus 1 Glycoprotein B Exhibits Altered Neurotropism and Increased Neurovirulence

2000 ◽  
Vol 74 (2) ◽  
pp. 817-827 ◽  
Author(s):  
Volker Gerdts ◽  
Jörg Beyer ◽  
Béla Lomniczi ◽  
Thomas C. Mettenleiter
Keyword(s):  
Respiratory Symptoms ◽  
Pseudorabies Virus ◽  
Bovine Herpesvirus ◽  
Glycoprotein B ◽  
Target Cells ◽  
Homologous Gene ◽  
Wild Type ◽  
Bovine Herpesvirus 1 ◽  
Herpesvirus 1

ABSTRACT Herpesvirus glycoproteins play dominant roles in the initiation of infection of target cells in culture and thus may also influence viral tropism in vivo. Whereas the relative contribution of several nonessential glycoproteins to neurovirulence and neurotropism ofPseudorabies virus (PrV), an alphaherpesvirus which causes Aujeszky's disease in pigs, has recently been uncovered in studies using viral deletion mutants, the importance of essential glycoproteins is more difficult to assess. We isolated an infectious PrV mutant, PrV-9112C2, which lacks the gene encoding the essential PrV glycoprotein B (gB) but stably carries in its genome and expresses the homologous gene of bovine herpesvirus 1 (BHV-1) (A. Kopp and T. C. Mettenleiter, J. Virol. 66:2754–2762, 1992). Apart from exhibiting a slight delay in penetration kinetics, PrV-9112C2 was similar in its growth characteristics in cell culture to wild-type PrV. To analyze the effect of the exchange of these homologous glycoproteins in PrV's natural host, swine, 4-week-old piglets were intranasally infected with 106 PFU of either wild-type PrV strain Kaplan (PrV-Ka), PrV-9112C2, or PrV-9112C2R, in which the PrV gB gene was reinserted instead of the BHV-1 gB gene. Animals infected with PrV-Ka and PrV-9112C2R showed a similar course of disease, i.e., high fever, marked respiratory symptoms but minimal neurological disorders, and excretion of high amounts of virus. All animals survived the infection. In contrast, animals infected with PrV-9112C2 showed no respiratory symptoms and developed only mild fever. However, on day 5 after infection, all piglets developed severe central nervous system (CNS) symptoms leading to death within 48 to 72 h. Detailed histological analyses showed that PrV-9112C2R infected all regions of the nasal mucosa and subsequently spread to the CNS preferentially by the trigeminal route. In contrast, PrV-9112C2 primarily infected the olfactory epithelium and spread via the olfactory route. In the CNS, more viral antigen and significantly more pronounced histological changes resulting in more severe encephalitis were found after PrV-9112C2 infection. Thus, our results demonstrate that replacement of PrV gB by the homologous BHV-1 glycoprotein resulted in a dramatic increase in neurovirulence combined with an alteration in the route of neuroinvasion, indicating that the essential gB is involved in determining neurotropism and neurovirulence of PrV.

scholarly journals Intraspecific bovine herpesvirus 1 recombinants carrying glycoprotein E deletion as a vaccine marker are virulent in cattle

2006 ◽  
Vol 87 (8) ◽  
pp. 2149-2154 ◽  
Author(s):  
Benoît Muylkens ◽  
François Meurens ◽  
Frédéric Schynts ◽  
Frédéric Farnir ◽  
Aldo Pourchet ◽  
...  
Keyword(s):  
High Frequency ◽  
Bovine Herpesvirus ◽  
Clinical Score ◽  
Natural Host ◽  
Field Strain ◽  
Bovine Herpesvirus 1 ◽  
Glycoprotein E ◽  
Control Programmes ◽  
Herpesvirus 1

Vaccines used in control programmes of Bovine herpesvirus 1 (BoHV-1) utilize highly attenuated BoHV-1 strains marked by a deletion of the glycoprotein E (gE) gene. Since BoHV-1 recombinants are obtained at high frequency in experimentally coinfected cattle, the consequences of recombination on the virulence of gE-negative BoHV-1 were investigated. Thus, gE-negative BoHV-1 recombinants were generated in vitro from several virulent BoHV-1 and one mutant BoHV-1 deleted in the gC and gE genes. Four gE-negative recombinants were tested in the natural host. All the recombinants were more virulent than the gE-negative BoHV-1 vaccine and the gC- and gE-negative parental BoHV-1. The gE-negative recombinant isolated from a BoHV-1 field strain induced the highest severe clinical score. Latency and reactivation studies showed that three of the recombinants were reexcreted. Recombination can therefore restore virulence of gE-negative BoHV-1 by introducing the gE deletion into a different virulence background.

scholarly journals Phosphorylation of Bovine Herpesvirus 1 VP8 Plays a Role in Viral DNA Encapsidation and Is Essential for Its Cytoplasmic Localization and Optimal Virion Incorporation

2016 ◽  
Vol 90 (9) ◽  
pp. 4427-4440 ◽  
Author(s):  
Kuan Zhang ◽  
Robert Brownlie ◽  
Marlene Snider ◽  
Sylvia van Drunen Littel-van den Hurk
Keyword(s):  
Golgi Apparatus ◽  
Mammalian Cells ◽  
Cellular Localization ◽  
Bovine Herpesvirus ◽  
Wild Type ◽  
Viral Dna ◽  
Bovine Herpesvirus 1 ◽  
Virion Incorporation ◽  
Herpesvirus 1 ◽  
Two Stages

ABSTRACTVP8 is a major tegument protein of bovine herpesvirus 1 (BoHV-1) and is essential for viral replication in cattle. The protein undergoes phosphorylation after transcription through cellular casein kinase 2 (CK2) and a viral kinase, US3. In this study, a virus containing a mutated VP8 protein that is not phosphorylated by CK2 and US3 (BoHV-1-YmVP8) was constructed by homologous recombination in mammalian cells. When BoHV-1-YmVP8-infected cells were observed by transmission electron microscopy, blocking phosphorylation of VP8 was found to impair viral DNA encapsidation, resulting in release of incomplete viral particles to the extracellular environment. Consequently, less infectious virus was produced by the mutant virus than by wild-type (WT) virus. A comparison of mutant and WT VP8 by confocal microscopy revealed that mutant VP8 is nuclear throughout infection while WT VP8 is nuclear early during infection and is associated with the Golgi apparatus at later stages. This, together with the observation that mutant VP8 is present in virions, albeit in smaller amounts, suggests that the incorporation of VP8 may occur at two stages. The first takes place without the need for phosphorylation and before or during nuclear egress of capsids, whereas the second occurs in the Golgi apparatus and requires phosphorylation of VP8. The results indicate that phosphorylated VP8 plays a role in viral DNA encapsidation and in the secondary virion incorporation of VP8. To perform these functions, the cellular localization of VP8 is adjusted based on the phosphorylation status.IMPORTANCEIn this study, phosphorylation of VP8 was shown to have a function in BoHV-1 replication. A virus containing a mutated VP8 protein that is not phosphorylated by CK2 and US3 (BoHV-1-YmVP8) produced smaller numbers of infectious virions than wild-type (WT) virus. The maturation and egress of WT and mutant BoHV-1 were studied, showing a process similar to that reported for other alphaherpesviruses. Interestingly, lack of phosphorylation of VP8 by CK2 and US3 resulted in reduced incorporation of viral DNA into capsids during mutant BoHV-1 infection, as well as lower numbers of extracellular virions. Furthermore, mutant VP8 remained nuclear throughout infection, in contrast to WT VP8, which is nuclear at early stages and Golgi apparatus associated late during infection. This correlates with smaller amounts of mutant VP8 in virions and suggests for the first time that VP8 may be assembled into the virions at two stages, with the latter dependent on phosphorylation.

scholarly journals Molecular modeling of HIV-1 reverse transcriptase drug-resistant mutant strains: implications for the mechanism of polymerase action

1997 ◽  
Vol 10 (12) ◽  
pp. 1379-1383 ◽  
Author(s):  
M. B. Kroeger Smith ◽  
C. J. Michejda ◽  
S. H. Hughes ◽  
P. L. Boyer ◽  
P. A. Janssen ◽  
...  
Keyword(s):  
Molecular Modeling ◽  
Reverse Transcriptase ◽  
Resistant Mutant ◽  
Drug Resistant ◽  
Mutant Strains ◽  
Drug Resistant Mutant ◽  
Hiv 1

scholarly journals A glycoprotein E deletion mutant of bovine herpesvirus 1 infects the same limited number of tissues in calves as wild-type virus, but for a shorter period

1995 ◽  
Vol 76 (9) ◽  
pp. 2387-2392 ◽  
Author(s):  
F. A. C. van Engelenburg ◽  
M. J. Kaashoek ◽  
J. T. van Oirschot ◽  
F. A. M. Rijsewijk
Keyword(s):  
Deletion Mutant ◽  
Bovine Herpesvirus ◽  
Wild Type Virus ◽  
Type Virus ◽  
Wild Type ◽  
Bovine Herpesvirus 1 ◽  
Glycoprotein E ◽  
Herpesvirus 1

Characterization of a spontaneous drug-resistant mutant of monkey B virus (Macacine herpesvirus 1)

2009 ◽  
Vol 154 (9) ◽  
pp. 1495-1497
Author(s):  
Darla H. Black ◽  
Lara K. Maxwell ◽  
R. Eberle
Keyword(s):  
Resistant Mutant ◽  
Drug Resistant ◽  
B Virus ◽  
Drug Resistant Mutant ◽  
Herpesvirus 1 ◽  
Monkey B Virus

scholarly journals Discovery of Novel Dual Inhibitors of the Wild-Type and the Most Prevalent Drug-Resistant Mutant, S31N, of the M2 Proton Channel from Influenza A Virus

2013 ◽  
Vol 56 (7) ◽  
pp. 2804-2812 ◽  
Author(s):  
Jizhou Wang ◽  
Chunlong Ma ◽  
Jun Wang ◽  
Hyunil Jo ◽  
Belgin Canturk ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Resistant Mutant ◽  
Proton Channel ◽  
Drug Resistant ◽  
Wild Type ◽  
Drug Resistant Mutant ◽  
Dual Inhibitors ◽  
M2 Proton Channel

Truncated bovine herpesvirus-1 glycoprotein I (gpI) initiates a protective local immune response in its natural host

Vaccine ◽  
1994 ◽  
Vol 12 (2) ◽  
pp. 145-152 ◽  
Author(s):  
Yi Gao ◽  
Thomas P. Leary ◽  
Linda Eskra ◽  
Gary A. Splitter
Keyword(s):  
Immune Response ◽  
Bovine Herpesvirus ◽  
Natural Host ◽  
Local Immune Response ◽  
Bovine Herpesvirus 1 ◽  
Glycoprotein I ◽  
Herpesvirus 1
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