Herpes simplex virus has developed the unique abilities of latency and neurovirulence. An important contributing factor in the strategy that enables these unique abilities is the inhibition of autophagy. Autophagy is a process that takes part in the maintenance of cell homeostasis in normal conditions, a disfunctional autophagy mechanism is linked to a variety of illneses like osteoarthritis and cancer. When the cell is undergoing a state of infection, autophagy takes part in the defence of the cell from intracellular pathogens. Many viruses have adapted to it in order to improve the chances of successful propagation. These viruses have evolved proteins which act upon the autophagic process and modulate intracellular signaling in order to hijack the mechanism of autophagy. The herpes simplex virus has evolved two proteins which have an effect on autophagy: ICP 34.5 is a part of the viral tegument and it inhibits autophagy directly at the onset of the viral infection. The other protein is Us11, which is typically found later during the infection, after transcription of viral genes and DNA replication has already started. Us11 ensures that the cellular sensors responsible for detecting foreign viral components in the citosole don`t trigger autophagy as a response to viral DNA. The importance of autophagy inhibition on the infection is evident in the fact that HSV-1 mutants lacking the forementioned proteins can rarely establish neurovirulence and neurolatency.