Analysis of equid herpesvirus 1 strain variation reveals a point mutation of the DNA polymerase strongly associated with neuropathogenic versus nonneuropathogenic disease outbreaks.

Nugent, J.; Birch-Machin, I.; Smith, K. C.; Mumford, J. A.; Swann, Z.; Newton, J. R.; Bowden, R. J.; Allen, G. P.; Davis-Poynter, N.

doi:10.1128/jvi.80.8.4047-4060.2006

Cited by 300Herpesvirus Infections and TreatmentsAnimal Virus Infections StudiesVirology and Viral Diseases

Analysis of equid herpesvirus 1 strain variation reveals a point mutation of the DNA polymerase strongly associated with neuropathogenic versus nonneuropathogenic disease outbreaks.

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Nugent, J., Birch-Machin, I., Smith, K. C., Mumford, J. A., Swann, Z., Newton, J. R., Bowden, R. J., Allen, G. P. +1 more·2006·Journal of Virology

DOI 10.1128/jvi.80.8.4047-4060.2006PMC PMC1440451

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Abstract

Equid herpesvirus 1 (EHV-1) can cause a wide spectrum of diseases ranging from inapparent respiratory infection to the induction of abortion and, in extreme cases, neurological disease resulting in paralysis and ultimately death. It has been suggested that distinct strains of EHV-1 that differ in pathogenic capacity circulate in the field. In order to investigate this hypothesis, it was necessary to identify genetic markers that allow subgroups of related strains to be identified. We have determined all of the genetic differences between a neuropathogenic strain (Ab4) and a nonneuropathogenic strain (V592) of EHV-1 and developed PCR/sequencing procedures enabling differentiation of EHV-1 strains circulating in the field. The results indicate the occurrence of several major genetic subgroups of EHV-1 among isolates recovered from outbreaks over the course of 30 years, consistent with the proposal that distinct strains of EHV-1 circulate in the field. Moreover, there is evidence that certain strain groups are geographically restricted, being recovered predominantly from outbreaks occurring in either North America or Europe. Significantly, variation of a single amino acid of the DNA polymerase is strongly associated with neurological versus nonneurological disease outbreaks. Strikingly, this variant amino acid occurs at a highly conserved position for herpesvirus DNA polymerases, suggesting an important functional role.

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More than 86% of neuropathogenic outbreaks are caused by strains encoding D752 and more than 95% of non-neuropathogenic outbreaks were caused by virus strains encoding DNA pol N752.
“It was demonstrated that more than 86% of neuropathogenic outbreaks are caused by strains encoding D752 and more than 95% of non-neuropathogenic outbreaks were caused by virus strains encoding DNA pol N752.”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Nugent et al., 2006
The Results report D752 in 42 of 49 neurological-outbreak isolates (86% when rounded) and N752 in 78 of 82 nonneurological-outbreak isolates (95% when rounded). The claim overstates the first percentage as “more than 86%” and describes the strains as causing the outbreaks, whereas the Discussion calls the finding an association and says a causal link had not been established. (LLM, conf=0.90)
Experimental — accuracy not yet measured
The neurovirulent EHV-1 strain presents a single nucleotide polymorphism in the catalytic subunit of the viral DNA polymerase ORF30, causing a substitution of asparagine by aspartic acid at amino acid position 752.
“The neurovirulent EHV-1 strain presents a single nucleotide polymorphism (SNP) in the catalytic subunit of the viral DNA polymerase (ORF30), causing a substitution of asparagine (N) by aspartic acid (D) at amino acid position 752 (Nugent et al., 2006).”
From The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1 (2021) · cites this paper as Nugent et al., 2006

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Comparative analysis of the genomes
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The ORF37 (UL24) is a neuropathogenicity determinant of equine herpesvirus 1 (EHV-1) in the mouse encephalitis model
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Pharmacokinetics of valacyclovir in the adult horse
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Equine Herpesvirus-1 Myeloencephalopathy, an Emerging Threat of Working Equids in Ethiopia
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Investigation of an EHV-1 Outbreak in the United States Caused by a New H752 Genotype
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Two outbreaks of neuropathogenic equine herpesvirus type 1 with breed‐dependent clinical signs
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Molecular Characterisation of Equine Herpesvirus 1 Isolates from Cases of Abortion, Respiratory and Neurological Disease in Ireland between 1990 and 2017
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Intranasal IgG4/7 antibody responses protect horses against equid herpesvirus-1 (EHV-1) infection including nasal virus shedding and cell-associated viremia
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A review of equid herpesvirus 1 for the veterinary practitioner. Part B: pathogenesis and epidemiology
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Prevalence of latent alpha-herpesviruses in Thoroughbred racing horses
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An Equine Herpesvirus Type 1 (EHV-1) Ab4 Open Reading Frame 2 Deletion Mutant Provides Immunity and Protection from EHV-1 Infection and Disease
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Phylogenetic and recombination analysis of the herpesvirus genus varicellovirus
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Equid herpesvirus 8: Complete genome sequence and association with abortion in mares
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Equine Herpesvirus-1 Outbreak During a Show-Jumping Competition: A Clinical and Epidemiological Study
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Identification of a New Equid Herpesvirus 1 DNA Polymerase (ORF30) Genotype with the Isolation of a C2254/H752 Strain in French Horses Showing no Major Impact on the Strain Behaviour
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New Real-Time PCR Assay Using Allelic Discrimination for Detection and Differentiation of Equine Herpesvirus-1 Strains with A 2254 and G 2254 Polymorphisms
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Updated ACVIM consensus statement on equine herpesvirus-1
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Emerging Infections: A Tribute to the One Medicine, One Health Concept
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Equine herpesvirus type-1 modulates CCL2, CCL3, CCL5, CXCL9, and CXCL10 chemokine expression
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Equine Herpesvirus 1 Bridles T Lymphocytes To Reach Its Target Organs
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Equine Herpesvirus-1 Myeloencephalopathy
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Meningitis and Encephalomyelitis in Horses
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Equid Herpesvirus Type-1 Exhibits Neurotropism and Neurovirulence in a Mouse Model
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Neonatal Immunization with a Single IL-4/Antigen Dose Induces Increased Antibody Responses after Challenge Infection with Equine Herpesvirus Type 1 (EHV-1) at Weanling Age
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A point mutation in a herpesvirus polymerase determines neuropathogenicity.
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Authors: Nugent, J., Birch-Machin, I., Smith, K. C., Mumford, J. A., Swann, Z., Newton, J. R., Bowden, R. J., Allen, G. P., & Davis-Poynter, N.
Affiliations: Animal Health Trust (GB)
Animal Health Trust, Kentford, Newmarket, United Kingdom
University of Oxford (GB)
University of Kentucky (US)
Corresponding author: Davis-Poynter, N.
ORCID: Newton, J. R.
Bowden, R. J.
Allen, G. P.
Davis-Poynter, N.
Venue: Journal of Virology
Publisher: American Society for Microbiology
Published: 2006-04-15
Volume: 80
Issue: 8
Pages: 4047-4060
ISSN: 0022-538X (ISSN-L)
1098-5514
DOI: 10.1128/jvi.80.8.4047-4060.2006
PMC: PMC1440451
OpenAlex: W2167022679
Cited by: 295
References: 60
Citations by year: 2026: 2 · 2025: 13 · 2024: 14 · 2023: 9 · 2022: 15 · 2021: 20 · 2020: 14 · 2019: 23 · 2018: 11 · 2017: 20 · 2016: 11 · 2015: 15 · 2014: 14 · 2013: 15 · 2012: 15
FWCI: 10.74
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Journal of Virology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Epidemiology › Herpesvirus Infections and Treatments
Life Sciences › Agricultural and Biological Sciences › Animal Science and Zoology › Animal Virus Infections Studies
Health Sciences › Medicine › Epidemiology › Virology and Viral Diseases
Keywords: equine herpesvirus 1, neurovirulence, genetic subgroups, strain differentiation, neurological disorders, equine herpesvirus
MeSH terms: Amino Acid Sequence, Animals, Base Sequence, Disease Outbreaks, DNA-Directed DNA Polymerase, Herpesvirus 1, Equid, Horse Diseases, Horses, Molecular Sequence Data, Open Reading Frames, Point Mutation, Polymorphism, Single Nucleotide

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Analysis of equid herpesvirus 1 strain variation reveals a point mutation of the DNA polymerase strongly associated with neuropathogenic versus nonneuropathogenic disease outbreaks.

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