Disease relevance of Herpesvirus 1, Equid

• The equine herpesvirus 1 glycoprotein gp21/22a, the herpes simplex virus type 1 gM homolog, is involved in virus penetration and cell-to-cell spread of virions [1].
• These results indicate that expression in vaccinia virus vectors of EHV-1 gp13, the glycoprotein homolog of herpes simplex virus gC-1 and gC-2, pseudorabies virus gIII, and the varicella-zoster virus gpV may provide useful vaccine candidates for equine herpesvirus infections [2].
• Genes for five EHV-1 glycoproteins (gp2, gp10, gp13, gp14, and gp21/22a) mapped to the genome L component; only one EHV-1 glycoprotein (gp17/18) was expressed from the unique S region of the genome where genes of several major glycoproteins of other herpesviruses have been located [3].
• A viral mutant (L11deltagM) bearing an Escherichia coli lacZ gene inserted into the EHV-1 strain RacL11 gM gene (open reading frame 52) was purified, and cells infected with L11deltagM did not contain detectable gM [1].
• The equine herpesvirus 1 (EHV-1) gene encoding glycoprotein 13 (gp13) was cloned into the hemagglutinin (HA) locus of vaccinia virus (Copenhagen strain) [2].

High impact information on Herpesvirus 1, Equid

• We have identified the equine herpesvirus 1 (EHV-1) thymidine kinase gene (TK) by DNA-mediated transformation and by DNA sequencing [4].
• The equine herpesvirus 1 UL20 product interacts with glycoprotein K and promotes egress of mature particles [5].
• These results suggested that the NREBP may mediate the NRE activity of the EICP0 promoter and may function in the coordinate expression of EHV-1 genes [6].
• Interaction of the equine herpesvirus 1 EICP0 protein with the immediate-early (IE) protein, TFIIB, and TBP may mediate the antagonism between the IE and EICP0 proteins [7].
• Mapping the sequences that mediate interaction of the equine herpesvirus 1 immediate-early protein and human TFIIB [8].

Chemical compound and disease context of Herpesvirus 1, Equid

• There have been conflicting reports regarding the gene assignment of the high-molecular-mass envelope glycoprotein gp2 (gp300) of equine herpesvirus 1 [9].
• A 1.4-kb mRNA appears initially at 2 h postinfection and is an early transcript since its synthesis is not affected by the presence of phosphonoacetic acid, an inhibitor of EHV-1 DNA replication [10].
• Effective chemotherapy of equine herpesvirus 1 by phosphonylmethoxyalkyl derivatives of adenine demonstrated in a novel murine model for the disease [11].
• One interpretation of these data is that EHV-1 gB is cleaved internally at both sites, a possibility which was supported by the apparent molecular masses of the unglycosylated gB subunits produced in the presence of tunicamycin [12].
• Induction of deoxythymidine kinase activity in several mammalian cell lines after infection with six different strains of equine herpesvirus type 1 (EHV-1) [13].

Biological context of Herpesvirus 1, Equid

• Wild-type equine herpesvirus 1 (EHV-1) strains express a large (250-kDa) glycoprotein, gp2, that is encoded by EUs4 (gene 71) located within the unique short region of the genome [14].
• The EICP0 protein of equine herpesvirus 1 (EHV-1) is an early, viral regulatory protein that independently trans-activates EHV-1 immediate-early (IE), early, gamma1 late, and gamma2 late promoters [15].
• Using PCR and nucleotide sequence analysis, it was shown that the ORF 71 genes of EHV-1 and EHV-4 are polymorphic due to a variable number of reiterated sequences in two regions, designated regions A and B. Region A was threonine-rich and was located near the N terminus [16].
• It was found that gp2, gp13, gp14, gp18 and a glycoprotein at 120K (EHV-1) or 116K (EHV-4) were all important immunogens in mares following EHV-1-induced abortion, and in a specific pathogen-free foal experimentally infected with EHV-1 and later cross-challenged with EHV-4 [17].
• Using transient transfections and chloramphenicol acetyltransferase assays the IE promoter of EHV-1 was shown to be trans-activated by VmW65 within the region -685 to +73 [18].

Anatomical context of Herpesvirus 1, Equid

• IL-2 and equine chorionic gonadotrophin (eCG) initiated reactivation of equid herpesvirus-1 (EHV-1) from venous lymphocytes at a frequency of 1/10(-5) [19].
• Transfer of supernatants showed that IL-2 and eCG acted indirectly by causing the release of other mediators from adherent cells; these mediators then reactivated EHV-1 from T cells [19].
• In vitro reactivation of latent equid herpesvirus-1 from CD5+/CD8+ leukocytes indirectly by IL-2 or chorionic gonadotrophin [19].
• Our results suggest that, in common with other alpha-herpesviruses, EHV-1 can establish latency in central nervous system neurons and that the unique membrane glycoprotein encoded by EHV-1 gene 71 is nonessential for infection of neural tissues [20].
• These data show that the SMAA system is an effective way of presenting subviral components to the immune system and further emphasises the importance of including glycoprotein D as a component of a subunit EHV-1 vaccine [21].

Gene context of Herpesvirus 1, Equid

• Evolution of the herpes thymidine kinase: identification and comparison of the equine herpesvirus 1 thymidine kinase gene reveals similarity to a cell-encoded thymidylate kinase [4].
• Severe murine lung immunopathology elicited by the pathogenic equine herpesvirus 1 strain RacL11 correlates with early production of macrophage inflammatory proteins 1alpha, 1beta, and 2 and tumor necrosis factor alpha [22].
• The second ORF of 336 aa, located at map units 0.075 to 0.08, has a predicted molecular weight (MW) of 38 kDa with significant homology to glycoprotein K (gK) of HSV-1 (UL53), ORF5 of VZV and ORF6 of EHV-1 [23].
• Finally, functionally equivalent sequences were also found in the C-terminus of the catalytic subunits of human cytomegalovirus (RRLHL) and of equine herpesvirus-1 DNA polymerase (RRILH) [24].
• The T-helper 1 (Th1) type of immune response induced by EHV-1 gD DNA was maintained after the protein boost, despite the gD protein alone appearing to direct a Th2 response [25].

Analytical, diagnostic and therapeutic context of Herpesvirus 1, Equid

• The UL2-specific antiserum reacted in Western immunoblot and immunoprecipitation analyses with a 23-kDa polypeptide synthesized in cells infected with standard EHV-1 or DIP-enriched virus [26].
• Sequence analysis of a glycoprotein D gene homolog within the unique short segment of the EHV-1 genome [27].
• Northern blot and S1 nuclease analyses identified a single 0.9-kb mRNA species that first appears at 2 hr postinfection, and whose synthesis is reduced in the presence of phosphonoacetic acid, an inhibitor of EHV-1 DNA synthesis [28].
• Protection against EHV-1 challenge infection in the murine model after vaccination with various formulations of recombinant glycoprotein gp14 (gB) [29].
• This initial demonstration that immunoreactive EHV-1 glycoprotein D can be produced as a secreted polypeptide in the baculovirus system should provide reagents to assess the potential use of gD as a subunit vaccine in an animal model [30].

References