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Herpesviridae is a large family of DNA viruses, capable of infecting higher as well as lower vertebrates. To date, more than one hundred species have been isolated and identified, and new species are still being discovered. For many years mammalian herpesviruses have been of interest to researchers because of their prevalence and pathogenicity, as well as significant economic losses associated with herpesviral infections, especially in livestock. In the course of their evolution, herpesviruses have perfectly adapted to their hosts and have developed the ability to establish latency. For years, many diverse efforts have been made to eliminate herpesviral infections, but the vaccines produced are generally ineffective and do not provide protection against the establishment of latency. Therefore, further research on their pathogenesis and continuous monitoring are needed to prevent the occurrence and spread of herpesvirus infections, particularly in farm and companion animals.
Equine herpesvirus type 1 (EHV-1) is a major viral pathogen of horses, causing respiratory disease, abortions, and equine herpes myeloencephalopathy (EHM). Like other alphaherpesviruses, EHV-1 establishes latency in neurons, but mechanisms involved in this process are still elusive. In the present study, we used antiviral drug acyclovir (ACV) to completely suppress EHV-1 replication in primary murine neuron culture. Trichostatin A (TSA), a known chemical reactivator of other herpesviruses, was used to stimulate productive EHV-1 infection. Moreover, gene expression of some cytokines was simultaneously evaluated, in order to check, whether the maintenance conditions of such a model may influence host cell response. Changes observed in IFN-α, IFN-β, and IL-10 mRNA gene expression depended on the EHV-1 strain. Although infection with either of the two EHV-1 strains investigated led to in an increase in type I IFNs gene expression, only the neuropathogenic strain caused a decrease in anti-inflammatory IL-10 gene expression. Unlike EHV-1 infection, the addition of neither ACV nor TSA caused significant changes in the expression of the above genes. We may therefore conclude that the in vitro model presented in the study is suitable for detailed investigation of the host cell-virus relationship on the molecular level.
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