Summary. -In this study we investigated the relationship of equid herpesvirus 1 (EHV-1) infection to autophagy in primary culture of murine neurons. Infection with both Jan-E and Rac-H strains of EHV-1 resulted in the formation of autophagosomes in the cytoplasm during early stages of infection, while in late stages of infection autophagosomes were mainly concentrated around the nucleus what suggests the induction of nuclear envelope-derived autophagy (NEDA). No significant effect of an authophagy inhibitor-chloroquine on final virus titers demonstrated that autophagy is not essential for EHV-1 replication.
Viruses are a very "clever" group of pathogens and well known for disrupting multiple processes in host cells. One of them is autophagy, a conserved mechanism that relies on degradation of intracellular structures in lysosomes. Autophagy can be triggered in response to viral infections and its aim is to digest viral particles, thereby limiting virus replication and spread. Induction of autophagy during viral infections is mediated by different regulatory pathways, but the biggest participation belongs to PKR and eIF2alpha. In this review we focused on the herpesvirus interactions with autophagic machinery. The Herpesviridae family presents various strategies to manipulate autophagy induction or suppression of that process may depend on cell type and stage of infection. Research carried out in the past 10 years has demonstrated the impact of herpesviruses on autophagy not only during productive infections, but in latency infections also.
Apoptosis is a process of programmed cell death in response to various stimuli, including virus infection. Herpesviruses have evolved the ability to interfere with apoptosis by its inhibition or activation in host cells. They can interfere with the extrinsic and intrinsic pathways of apoptosis. A special feature of herpesviruses is establishing a latent infection, during which expression of virus genes is strongly restricted and production of infectious virus particles is not observed. HSV-1 establishes latency in neurons, CMV in bone marrow progenitor cells and monocytes, EBV and HHV-8 in B cells. Studies show that latent infections also depend on prevention of the death of the infected cells. Control of apoptosis machinery by viruses may be critical for their reproduction and provision of the adequate yield of progeny virions. The present article summarizes the current knowledge about the latent viral infection and mechanisms of apoptosis modulation by selected viruses from the Herpesviridae family.
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