The effect of in vitro and in vivo serial virus passage on the genetic stability of equine herpesvirus 1 (EHV-1) was investigated by restriction endonuclease analysis of the viral DNA. It is a major constituent of the DNA of EHV-1 defective-interfering (DI) particles which have been shown to mediate the coestablishment of oncogenic transformation and persistent infection of hamster embryo cells. These results indicate that point nucleotide differences in RacL11 and Kentucky D might be responsible for their pathogenicity in rodent models. After transfection of vL11ΔETIF DNA into RK13 cells, no infectious virus could be reconstituted, and only single infected cells or small foci containing up to eight infected cells were detected. Subsequently, similar studies characterized both integrated and free viral sequences in polyoma and BK virus transformed cells (3, 4, 5). For example, a new gene predicted in the genome of the Epstein–Barr virus was shown to encode a protein similar to α‐herpesvirus minor tegument protein UL14 with heat shock functions. (C) Depiction of genes 70 to 72 from the unique short region.
EHV-1 infection is ubiquitous in most horse populations throughout the world, and causes disease in horses and extensive economic losses through frequent outbreaks of respiratory disease, abortion, neonatal foal death, and myeloencephalopathy. Infections caused by EHV-1 are particularly common in young performance horses, and typically result in establishment of latent infection within the 1st weeks or months of life with subsequent viral reactivation causing clinical disease and viral shedding during periods of stress. Sporadic occurrence of mild respiratory disease associated with pyrexia, principally affecting horses under 2 years of age, can lead to interruptions in athletic training programs; this is economically the least important manifestation of EHV-1 disease. Abortion occurring during the 3rd trimester of pregnancy, results in important economic losses. Outbreaks of neurological disease (equine herpes myeloencephalopathy or EHM) cause suffering and loss of life and also lead to extensive movement restrictions, disrupting breeding or training schedules and causing management difficulties at training centers, race tracks, and horse events. We also detected an eight bp inverted repeat sequence flanking the unique long segment of the SVV genome (Mahalingam et al., 2000). CBC showed neutrophilia (11.6 × 103/uL; reference range: 2.6–5.5 × 103/uL), monocytosis (0.46 × 103/uL; reference range: 0–0.35 × 103/uL), and hyperfibrinogenemia (500 mg/dL; reference range: 100–400 mg/dL).
Thus, EHV-9 has the potential to spread other hosts. The a sequence is necessary and sufficient to direct cleavage and packaging of HSV-1 genomes (31–33). The air around a horse that is shedding the virus can also be contaminated with infectious virus. Subdivide horses into the small epidemiologically isoated closed groups. The initial step in the formation of a preinitiation complex is the assembly of the TFIID–TFIIA (D–A) complex at the TATA box element (reviewed in Hampsey, 1998). Maximize herd immunity through vaccination. Therefore, strain Wh is genetically closer to EHV-9 than to EHV-1.
Isolation of affected horses. Submission of clinical samples to a diagnostic laboratory. Implementation of hygienic procedures to prevent spread of infection (biosecurity).