Herpesviral Diseases of the Horse

Bryans, J T; Allen, George P.

doi:10.1007/978-1-4613-1587-2_6

Cited by 44 publications

(45 citation statements)

References 70 publications

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“…Replication is followed by a leukocyte-associated viremia which enables EHV-1 to reach internal organs. There, its replication can result in abortion, neonatal death or nervous system disorders (Allen and Bryans, 1986;Bryans and Allen, 1989). Abortion can involve only one or two mares in a herd but also abortion storms can occur on a premise, associated with great economic losses (Allen and Bryans, 1986).…”

Section: Introductionmentioning

confidence: 99%

In vitro susceptibility of six isolates of equine herpesvirus 1 to acyclovir, ganciclovir, cidofovir, adefovir, PMEDAP and foscarnet

Garré

Meulen

Nugent

et al. 2007

Veterinary Microbiology

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Equine herpesvirus 1 (EHV-1) is an important equine pathogen that causes respiratory disease, abortion, neonatal death and paralysis. Although vaccines are available, they are not fully protective and outbreaks of disease may occur in vaccinated herds. Therefore, there is an urgent need for effective antiviral treatment. For three abortigenic (94P247, 97P70 and 99P96) and three neuropathogenic isolates (97P82, 99P136 and 03P37), the effect of acyclovir, ganciclovir, cidofovir, adefovir, 9-(2-phosphonylmethoxyethyl)-2,6-diaminopurine (PMEDAP) and foscarnet on plaque number was studied. Additionally, for isolate 97P70, the effect on plaque size was investigated. Ganciclovir was most potent in reducing plaque number, followed by PMEDAP and acyclovir. Adefovir and cidofovir were less effective and foscarnet was the least effective compound. There were no differences detected for acyclovir, ganciclovir, adefovir and PMEDAP between the abortigenic and neuropathogenic isolates. One abortigenic isolate (99P96) was more susceptible to cidofovir and two neuropathogenic isolates (99P136 and 03P37) were less susceptible to foscarnet. For isolate 97P70, all compounds resulted in a significant reduction of plaque size. The most remarkable effect was observed for cidofovir. It was 40-fold more effective in reducing plaque size than in reducing plaque number. In conclusion, ganciclovir was the most potent compound and therefore, may be a valuable candidate for the treatment of EHV-1 infections in horses. The antiviral effect of foscarnet on plaque number was highly dependent on the viral isolate tested. Therefore, it is no valuable antiviral for the treatment of herpesvirus-infections. Cidofovir, although less effective in reducing plaque number, had a strong effect on plaque size. #

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Section: Introductionmentioning

confidence: 99%

In vitro susceptibility of six isolates of equine herpesvirus 1 to acyclovir, ganciclovir, cidofovir, adefovir, PMEDAP and foscarnet

Garré

Meulen

Nugent

et al. 2007

Veterinary Microbiology

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“…as neurological symptoms originate mainly from virus replication in the endothelium of small blood vessels and related minor extravasations and thrombosis (Bryans et al 1989, Sauerbrei et al 2002. Although many studies have been devoted to the pathogenesis of various clinical forms of EHV-1 infection, it is still not fully explained how EHV-1 can damage cells.…”

mentioning

confidence: 99%

Equine herpesvirus type 1 (EHV-1) replication in primary murine neurons culture

Cymerys

Dzieciątkowski²,

Słońska³

et al. 2010

Polish Journal of Veterinary Sciences

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Equine herpesvirus-1 (EHV-1) infections cause significant economic losses for equine industries worldwide as a result of abortion, respiratory illness, and neurologic disease in all breeds of horses. The occurrence of abortions caused by EHV-1 has repeatedly been confirmed in Poland, but neurological manifestations of the infection have not been described yet. Also it is unknown how the infection of neurons with non-neuropathogenic strains is regulated. To further understand the virus-neuron interaction we studied two strains of EHV-1 in murine primary neuron cell cultures. Both strains were isolated from aborted fetuses: Rac-H, a reference strain isolated by Woyciechowska in 1959 (Woyciechowska 1960) and Jan-E isolated by Bańbura et al. (Bańbura et al. 2000). Upon infection of primary murine neuronal cell cultures with Jan-E or Rac-H strains, a cytopathic effect was observed, manifested by a changed morphology and disintegration of the cell monolayer. Positive results of immunofluorescence, nPCR and real-time PCR tests indicated high virus concentration in neurons, meaning that both EHV-1 strains were likely to replicate in mouse neurons in vitro without the need for adaptation. Moreover, we demonstrated that some neurons may survive (limited) virus replication during primary infection, and these neurons (eight weeks p.i.) harbour EHV-1 and were still able to transmit infection to other cells.

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“…Equine herpesvirus type 1 (EHV-1) causes an important infection in horses associated with a variety of clinical problems including respiratory distress, abortion (Bryans & Allen, 1989) and neurological signs (Charlton et al, 1976;Chowdury et al, 1986). The serologically related but distinct virus, EHV-4, also causes a common infection and both EHV-1 and EHV-4 establish latent infections in horses from which they may be reactivated.…”

mentioning

confidence: 99%

Cell-mediated antiviral response to equine herpesvirus type 1 demonstrated in a murine infection model by means of adoptive transfer of immune cells

Lila

Field

1993

Journal of General Virology

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Protection against equine herpesvirus type 1 (EHV-1) infection in a mouse model has been studied by means of delayed-type hypersensitivity (DTH) and adoptive transfer of immune spleen cells. Mice were found to develop a positive DTH response to EHV-1 antigen which was sustained for several months after primary inoculation. The response was found to cross-react with EHV-4-derived antigen. Immune cells (from mice primed with live or heat-inactivated EHV-1) conferred an enhanced DTH response on recipients; however, only the immune cells that were previously primed with live EHV-1 gave protection against re-infection. The degree of protection was also dependent on the number of spleen cells transferred. Immune cells from mice primed with heatinactivated EHV-1 appeared to enhance virus replication following subsequent inoculation. The serum antibody response to EHV-1 appeared to be slightly suppressed in recipients of spleen cells from mice primed with either live or heat-inactivated virus. These results support the important role for cell-mediated responses in protective immunity to EHV-1 and provide clues to the nature of protection and immunopathology in the natural host.

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Herpesviral Diseases of the Horse

Cited by 44 publications

References 70 publications

In vitro susceptibility of six isolates of equine herpesvirus 1 to acyclovir, ganciclovir, cidofovir, adefovir, PMEDAP and foscarnet

In vitro susceptibility of six isolates of equine herpesvirus 1 to acyclovir, ganciclovir, cidofovir, adefovir, PMEDAP and foscarnet

Equine herpesvirus type 1 (EHV-1) replication in primary murine neurons culture

Cell-mediated antiviral response to equine herpesvirus type 1 demonstrated in a murine infection model by means of adoptive transfer of immune cells

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