Microbiology Society Journals | Glycoprotein 60 of equine herpesvirus type 1 is a homologue of

J. Equine herpesvirus type 1 (EHV-1) is a major pathogen affecting horses worldwide. Dr. Affected foals are occasionally born alive, but they are generally very weak and succumb within days of birth, often with secondary disease conditions. These findings give new insights into the complex pathogenesis of EHV-1. If your testimonial is selected for our website showcase, you’ll receive 1,000 EzCoupon™ points. Procoagulant activity was mildly decreased (30-40%) when virus was inactivated by ultraviolet light or when infected cells were treated with aphidicolin, a virus DNA polymerase inhibitor, suggesting early events of virus infection (attachment, entry or intracellular trafficking) are the primary stimulus of procoagulant activity.

Ab4 infection resulted in a significant reduction of IL-10 responses in adult horses. Pre-treatment of CD172a(+) cells with inhibitors of histone deacetylase activity increased and accelerated viral protein expression at very early times of infection and induced productive infection in CD172a(+) cells. Analyses of host gene expression showed that a subset of pro-inflammatory cytokines, including the CXCR3 ligands CXCL9, CXCL10, and CXCL11, as well as CCL5, IL-6 and TNF-α were consistently up-regulated in endothelial cells infected with each EHV-1 strain. It was not reactive with common opportunistic pathogens such as Escherichia coli, Klebsiella oxytoca, Pseudomonas aeruginosa and Enterobacter agglomerans often involved in abortion. This may not be the complete list of references from this article. The EHM variant is considered neuropathogenic due to its ability to replicate to higher viremic titers and cause higher neurologic morbidity and mortality as compared to the wild type EHV1. An identical deletion of 0.85 kbp in size was found in both copies of the inverted repeat (IR) regions of RacH.

In addition, a poorly resolved glucosamine-rich region (mol. Our findings suggest that the ORF59 protein plays a major role in EHV-1 replication in vitro and likely in vivo. Additional experiments performed without the use of metabolic inhibitors confirmed that EHV-1 transcription is temporally regulated. The vaccine strain differed from other isolates investigated with 4 restriction endonucleases (Bam HI, Bgl II, EcoRI, Kpn I) which was due to a deletion in the unique short segment of the genome. The detection limit of the assay was shown to be 6.0 × 10⁰ of viral DNA copies and the obtained standard curve exhibited a linear range from 10⁰ to 10⁷ molecules. All mares in both groups exhibited nasal viral shedding and viremia. The EHV-1-induced enzyme utilized both ATP and CTP as phosphate donors and differed in relative electrophoretic mobility from the TKs of mock-infected and HSV-1-infected cells.

One BamHI site located in the ribosyl reductase gene was missing in RacH, RacM24, RacM36, and RacL22; and 2. Here we examined whether differences in the immunomodulatory glycoprotein G (gG) between the two viruses determine EHV-1’s ability to cause systemic infection. Twenty-two of these ICPs comigrated with virion structural proteins. When EGFP-fused VP22 was overexpressed in the cells, VP22 localized in the cytoplasm and nucleus. Here, we constructed an EHV-1 VP22 deletion mutant and a revertant virus to clarify the role of VP22. This report describes the first detection of EHV-1 DNA in neonatal dead foals by using the genetic method in Turkey. The gB4-containing-EHV-1 (EHV-1_gB4) recombinant virus was analyzed for growth in culture, cell tropism, and cell entry rivaling no significant differences when compared to parental virus.

ORF34 protein (pORF34)-specific antibodies specifically reacted with a 28-kDa early polypeptide present in the cytosol of infected cells. The diagnosis of EHV-1 myeloencephalitis was supported by postmortem findings, PCR identification of the virus and by serological tests with an EHV-1 -specific ELISA. The full genome sequences of the 3 strains were determined. Environmental, viral, and host risk factors might contribute to neurological manifestation. The equine herpesvirus type 1 (EHV-1) immediate-early (IE) gene encodes a phosphoprotein that is essential for the activation of transcription from viral early and late promoters and that regulates the transcription from its own promoter. Recently, a type-specific ELISA using equine herpesvirus type 1 (EHV-1) and type 4 (EHV-4) glycoprotein Gs (gGs) was developed by Crabb and Studdert [1993]. Equine herpesvirus type 4 (EHV-4) is one of the most important pathogens in horses.

The serological relationship between a New Zealand strain of equine herpesvirus type 1 (EHV 1) isolated from the respiratory form of the disease, and one isolated from an aborted foetus was investigated. A peptide-based enzyme-linked immunosorbent assay (ELISA) for discrimination between serological responses to equine herpesvirus type 1 (EHV-1) and 4 (EHV-4) was developed. Equine herpesvirus type 1 (EHV-1) is a major cause of winter pyrexia in racehorses in two training centers (Ritto and Miho) in Japan. A strain of equine herpesvirus type 1 (EHV-1) was isolated from zebra. The objective of the investigations was to study the occurrence of the equine herpesvirus type 1 (EHV-1) infection in aborted equine fetuses and in newborn foals and to compare the sensitivity of virus isolation, immunohistochemistry and histology in 101 cases and of fetal serology in 68 cases in the diagnosis of the infection.

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