A game of survival: herpesvirus strategies of autophagy manipulation.

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.

Autophagy in cultured murine neurons infected with equid herpesvirus 1.

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.

[Herpesviruses survival strategies--latency and apoptosis].

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.