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Here, we constructed an EHV-1 VP22 deletion mutant and a revertant virus to clarify the role of VP22. Of the 113 cases analyzed, 3 (2.7%) were induced by ORF30 G2254 strains. The exceptional respiratory isolate, EHV1 Army 183, had a foetal (F) strain fingerprint but this virus cannot be said with certainty to have been isolated from the respiratory tract. We have adapted the polymerase chain reaction (PCR) to detect and distinguish between EHV-1 and EHV-4 in the same reaction. The detection limit of the LAMP assay with heat treatment was 10 times more sensitive than the original LAMP assay even when the DNA extraction step was omitted. In this report, we present the DNA sequence and tran-scriptional characterization of a gene (IR3) that maps entirely within the IR sequences. The initial rate of reassociation of either labeled viral DNA was increased by the presence of the heterologous viral DNA to an extent indicating only 2 to 5% homology between the two EHV genomes.

These results suggest that both gI and gE contribute to the ability of EHV-1 to spread directly from cell-to-cell, but that these glycoproteins are not required for viral growth in vitro. cDNAs from this EHV-1-susceptible cell type were inserted into EHV-1-resistant B78H1 murine melanoma cells, these cells were infected with an EHV-1 lacZ reporter virus, and cells that supported virus infection were identified by X-Gal (5-bromo-4-chloro-3-indolyl-β-d-galactopyranoside) staining. The 42 strains of EHV-1 and 64 strains of EHV-4 were isolated from 4593 nasal swabs and/or blood plasma samples collected from 3326 horses during a period from 1979 to 1990. The video is now available on YouTube. One of the key questions central to such concerns is ‘how common is it for hospitalised horses to shed EHV-1?’ According to the results of a paper by Pusterla and others (2015) summarised on page 70 of this issue of Veterinary Record, only 2.7 per cent of 4228 horses from 139 veterinary practices throughout the USA tested positive for EHV-1 DNA in their nasal secretions or blood. Comparison of the EHV-1 DNA sequence with that encoding glycoproteins of other alphaherpesviruses has revealed no significant homologies. EHV-1 infections manifest in three syndromes: respiratory, reproductive and neurologic.

The positive strand and one negative strand primer were designed to encompass the deletions present in RacH, and the second negative strand primer was designed to hybridize within these deletions. The full genome sequences of the three strains were determined. Utilizing these powerful molecular tools, Ketner and Kelly (1) and Botchan et al. Determination of the nucleotide sequence of the DNA fragment revealed a complete transcriptional unit composed of typical regulatory promoter elements upstream to a long open reading frame (1,404 base pairs) that encoded a 468-amino-acid primary translation product of 51 kilodaltons. Of the 113 cases analyzed, 3 (2.7%) were induced by ORF30 G(2254) strains. Western blot analysis of mutated EHV-1 gB showed that it was cleaved at two positions, 518RRRR521 and 544RLHK547, and that the 28 aa between the two sites were removed after cleavage. In this paper, an attempt of real-time PCR has been described, which uses specific fluorochrome-labeled TaqMan probes for detection of viral DNA.

The deletion virus was then repaired to encode D752 or N752, respectively. However, the mechanism by which EHV-1 is transferred from CD172a+ cells to endothelial cells (EC) remains unclear. PROCEDURES: EHV-1 strain Ab4 was administered intranasally on day 0, and small interfering RNAs (siRNAs [EHV-1 specific siRNAs {n = 7} or an irrelevant siRNA {6}]) were administered intranasally 24 hours before and 12, 24, 36, and 48 hours after infection. We report here on an immunomodulatory protein involved in this process, pUL56, which is encoded by ORF1 of equine herpesvirus type 1 (EHV-1), an alphaherpesvirus. The efficiency of transfection (50 to 100 plaque-forming units/microgram of DNA) was reduced by treatment of the viral DNA with deoxyribonuclease or sonication but not with Pronase or antivirus neutralizing serum. A combination of nucleic acid precipitation and preamplification steps was used to increase the analytical sensitivity of the analysis. Transcription analyses have revealed that the EHV-1 IR sequence encodes at least 6 genes.

Infection of equine monocyte-derived DC (MDDC) with EHV1 induced down-regulation of major histocompatibility complex I (MHCI), CD83, CD86, CD206, CD29 and CD172a, but not of CD11a/CD18 and MHCII. These syndromes have been attributed to ischemic necrosis from thrombosis in placental and neural vessels, although the mechanisms underlying thrombosis are unknown. Northern blot analysis was used to characterize and map equine herpesvirus type 1 (EHV-1) immediate early (IE), early, and late transcripts. The recent increase in incidence, morbidity, and mortality of neurological disease induced by equine herpesvirus type 1 (EHV-1) has suggested a change of virulence of the virus. Equine herpesvirus type 9 (EHV-9), which we isolated from a case of epizootic encephalitis in a herd of Thomson’s gazelles (Gazella thomsoni) in 1993, has been known to cause fatal encephalitis in Thomson’s gazelle, giraffe, and polar bear in natural infections.