Abstract
Equine herpesvirus type 1 (EHV-1) causes respiratory disease, abortion and neurological disorders in horses. In the present study, we investigated reorganization of the cytoskeleton in neurons infected with two EHV-1 strains: Jan-E (wild-type strain) and Rac-H (attenuated strain). The studies were performed on primary murine neurons, which are an excellent model for studying neurotropism and neurovirulence of EHV-1. We have demonstrated for the first time that EHV-1 infection causes rearrangements in the actin network of neurons that are dependent on the virus strain and its adaptation to cell culture in vitro. Immunofluorescent labeling and confocal microscopy revealed the formation of long, thin projections in neurons infected with the Jan-E strain, which was probably associated with enhanced intracellular spread of the virus. The EHV-1 Rac-H strain caused disruption of the microfilaments system and general depolymerization of actin, but treatment of neurons with cytochalasin D or latrunculin A resulted in limitation of viral replication. It can therefore be assumed that actin filaments are required only at the early stages of infection. Our results allow us to suggest that the actin cytoskeleton participates in EHV-1 infection of primary murine neurons but is not essential, and that other components of the cytoskeleton and/or cellular mechanisms may be also involved during EHV-1 infection.
Highlights
Equine herpesvirus type 1 (EHV-1) is a member of the subfamily Alphaherpesvirinae of the family Herpesviridae
We have demonstrated for the first time that EHV-1 infection causes rearrangements in the actin network of neurons that are dependent on the virus strain and its adaptation to cell culture in vitro
The organization of actin filaments in EHV-1-infected and control neuronal murine cells was examined by confocal microscopy at 24, 48 and 72 h p.i
Summary
Equine herpesvirus type 1 (EHV-1) is a member of the subfamily Alphaherpesvirinae of the family Herpesviridae. It induces mild respiratory diseases, abortion, neonatal foal death, and neuropathogenic disorders. Like the other a-herpesviruses (HSV-1, BHV-1, PRV), EHV-1 infection is characterized by neurotropism and the ability to establish latent infections in trigeminal ganglion neurons [3, 16, 17, 19]. Viruses have evolved a broad spectrum of mechanisms to exploit the host cell, including actin filaments—one of the three major components of the cytoskeleton. Numerous studies have confirmed that various herpesviruses interact with the cell cytoskeleton throughout their life cycle, upon entry, replication or egress, disrupting and rearranging the actin filaments so they can utilize them as tracks or shove them aside when they represent barriers [4, 11, 14, 18, 22, 26]
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