Disease relevance of US8

• Glycoprotein E of HSV-1 has been shown to function as an Fc receptor [1].
• Pseudorabies virus (PRV) glycoprotein E (gE) is a type I viral membrane protein that facilitates the anterograde spread of viral infection from the peripheral nervous system to the brain [2].
• A mutant of herpes simplex virus type 1 lacking both glycoprotein M and glycoprotein E was marginally compromised in terms of its in vitro growth characteristics [3].
• Wild-type (WT) and gE-null (NS-gEnull) viruses both infected retina ganglion cell neurons; however, NS-gEnull viral antigens failed to reach the optic nerve, which indicates a defect in axonal localization [4].
• The purpose of this study was to determine whether individual milk samples can replace serum samples for the detection of bovine herpesvirus 1 (BHV1) glycoprotein E (gE)-specific antibodies [5].

High impact information on US8

• We used the mouse retina infection model and neuronal cell cultures to define the spread phenotype of gE mutant viruses [4].
• Herpes simplex virus type 1 glycoprotein e is required for axonal localization of capsid, tegument, and membrane glycoproteins [4].
• The site of the defect in retrograde spread remains to be determined; however, infection of rat superior cervical ganglia neurons in vitro indicates that gE is required to target virion components to the axon initial segment [4].
• Herpes simplex virus type 1 (HSV-1) glycoprotein E (gE) promotes cell-to-cell spread at basolateral surfaces of epithelial cells, but its activity in neurons is less clear [4].
• MDV gD could not be immunoprecipitated from MDV GA-infected duck embryo fibroblast cells by antisera reactive to its TrpE fusion proteins, while gI and gE could be [6].

Chemical compound and disease context of US8

• A role for bovine herpesvirus 1 (BHV-1) glycoprotein E (gE) tyrosine phosphorylation in replication of BHV-1 wild-type virus but not BHV-1 gE deletion mutant virus [7].
• A live attenuated glycoprotein E negative bovine herpesvirus 1 vaccine induces a partial cross-protection against caprine herpesvirus 1 infection in goats [8].

Biological context of US8

• 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 [9].
• The decrease in viral titer was directly proportional to the decrease in phosphorylation of the BHV-1 gE [7].
• This study focused on the correlation of the residual virulence of several VV recombinants with antibody responses against the strongly immunogenic extrinsic glycoprotein E of varicella-zoster virus and the weakly immunogenic extrinsic protein preS2-S of hepatitis B virus and against VV proteins, with mice used as a model organism [10].
• This was obtained by removing the complete gE coding region from the BHV-1 genome [11].
• Our results indicate that the tyrosine phosphorylation of the cytoplasmic tail of BHV-1 gE is an important post-translational modification of the functional protein [7].

Anatomical context of US8

• Five calves received at birth colostrum from gE-seronegative cows which had been vaccinated two or three times with an inactivated BHV-1, gE-deleted marker vaccine [12].

Associations of US8 with chemical compounds

• Inhibition of phosphorylation of BHV-1 gE by tyrosine kinase inhibitors genistein and tyrphostin AG1478 substantially lowered the viral titer in Madin-Darby bovine kidney cells [7].
• Results showed that the MAbs were directed against three antigenic domains, two located on the gE glycoprotein and one on the gE/gI complex [13].
• RESULTS: Genistein reduced BHV-1, but not gE-deleted BHV-1 (BHV-1gEdelta3.1), replication by 90% at 18 hours after inoculation [14].

Other interactions of US8

• An inactivated glycoprotein E-negative vaccine and an experimental glycoprotein D-subunit vaccine against bovine herpesvirus 1 (V1) were examined for their effectiveness in a randomized, double-bline, placebo-controlled field trial comprising 130 dairy farms [15].
• Virulence and immunogenicity in calves of thymidine kinase- and glycoprotein E-negative bovine herpesvirus 1 mutants [16].

Analytical, diagnostic and therapeutic context of US8

• In animal models, a gE-null mutant infection spreads inefficiently from presynaptic neurons to postsynaptic neurons (anterograde spread of infection) [2].
• In comparison to serum, the results showed that the gE-blocking ELISA was highly sensitive for testing milk samples (0.96) [5].
• Detection of bovine herpesvirus type 1 in blood from naturally infected cattle by using a sensitive PCR that discriminates between wild-type virus and virus lacking glycoprotein E [17].
• We demonstrated BHV-1 glycoprotein E (gE) to be the tyrosine phosphorylated viral protein by immunoprecipitation [7].
• The effects of the vaccination of neonatal calves with a glycoprotein E (gE)-negative bovine herpesvirus type 1 (BHV-1) were investigated in naïve and passively immunised calves either with the recommended dose or a 5-fold concentrated one [18].

References