New real-time PCR assay using allelic discrimination for detection and differentiation of equine herpesvirus-1 strains with A2254 and G2254 polymorphisms

Zebra-borne neurotropic equid herpesvirus 1 meningoencephalitis in a Thomson’s gazelle (Eudorcas thomsonii)

“…LM2014 was also tested for the presence or absence of the EHV-1-specific neuropathogenicity marker characterized by a non-synonymous nucleotide substitution (A-to-G) at a specific position in the polymerase gene (ORF30). 22 Similar to the reported findings for all 3 zebra-born EHV-1 strains (T-529, 94-137, and T-616), 12 LM2014 was found to bear that same marker. The sequence information derived from partial sequencing of ORF59/60 and a hypervariable region of the gG gene of the Thomson's gazelle-derived herpesvirus, LM2014, indicate that this virus is zebra-borne EHV-1-like and not EHV-9.…”

Third International Havemeyer Workshop on Equine Herpesvirus type 1

“…An outbreak of EHV‐1 occurred in Utah, USA in 2011 with 26 confirmed cases of EHM (http://www.aphis.usda.gov/vs/nahss/equine/ehv/ehv_2011_final_sitrep_062311.pdf). The relevant veterinary organisations recommended that owners of potentially exposed horses quarantined their animals and monitored and reported clinical disease promptly and this advice was followed effectively [17]. EHV‐1 isolates from neurological outbreaks show a consistent ORF30 D 752 genotype, but in non‐neurological outbreaks, the D 752 mutation can be present, along with nonsynonymous mutations in other areas of this gene [5,18–20]. These additional mutations may attenuate the effects of the D 752 genotype. The group unanimously rejected the notion that infection control during outbreaks from which ‘neurological’ and ‘non‐neurological’ genotypes of EHV‐1 are isolated should be different: robust biosecurity must be implemented for all EHV‐1 outbreaks, regardless of genotype, according to the Horserace Betting Levy Board's Codes of Practice (http://codes.hblb.org.uk/) and ACVIM Consensus Statement [1].…”

“…EHV‐1 isolates from neurological outbreaks show a consistent ORF30 D 752 genotype, but in non‐neurological outbreaks, the D 752 mutation can be present, along with nonsynonymous mutations in other areas of this gene [5,18–20]. These additional mutations may attenuate the effects of the D 752 genotype.…”

“…Multiple factors are responsible for the virulence of a particular isolate in an individual horse including the genes and proteins expressed by each virus isolate, the host's genetic background and immune status and response. Molecular techniques such as quantitative PCR and next generation sequencing now contribute routinely to the diagnosis and genotyping of EHV‐1 isolates collected from clinically infected horses during outbreaks [19,28]. Other techniques including microarray analyses of the transcriptomes are being applied to isolates of EHV‐1 which are associated with different clinical outcomes as well as cells from the equine host: these will elucidate the genes and pathways which may be up‐ or downregulated during infection.…”

Emergence of equine herpes virus 1 myeloencephalopathy: A brief review

“…Use of novel PCR platforms, such as real-time PCR assays based on ORF30 enable the differentiation of neuropathogenic and non-neuropathogenic viruses (Allen, 2007;Leutenegger et al, 2008). Single nucleotide polymorphism (SNP)-real-time PCR (Smith et al, 2012) and primer-probe energy transfer method (Malik et al, 2010) have been used for diagnosis of EHM. A SNP-based real-time PCR has been developed in our laboratory that is able to differentiate neuropathogenic and non-neuropathogenic EHV1 strains.…”