Host messenger RNAs can be modulated at various stages including pre-RNA processing, nuclear export or modification of RNA decay. Whatever the means, viral messenger RNAs rely on alternative ways to be expressed. For example, viruses shutting off host nuclear gene transcription or mRNA export are often transcribed in the cytoplasm. The main mechanism by which viruses inhibit host gene expression is by specifically targeting the translation of host mRNAs �C which requires proteins not used for translation of viral proteins. Viruses inhibiting cap dependent translation use an internal ribosome entry site or similar structures for translation initiation of their proteins. The protease 3C from enteroviruses cleaves host eiF5B while the protease from retroviruses cleaves eiF4G, completely abrogating cellular translation. Viral replication is limited by the ability of the host metabolic machinery to produce the resources �C nucleic acids and proteins �C necessary for the assembly of viral progeny. These resources are most abundant during the S-phase of the cell cycle, and many DNA viruses modulate the G1/S transition to initiate DNA synthesis. Viruses such as Epstein-Barr virus, human cytomegalovirus, adenoviruses and SV40 modulate the activity of retinoblastoma protein family members to drive cells in S-phase. Viruses infecting quiescent cells have also evolved mechanisms to force entry into the cell cycle. Myxomavirus MT5 Tianeptine sodium salt promotes phosphorylation, ubiquitination and BLZ945 degradation of the cyclin-dependent kinase inhibitor p27/KIP1. Viruses also retard the initiation of mitosis �C the G2/M transition �C to allow replication of their own genome before mitosis and sometimes to prevent clonal expansion of infected lymphocytes. Several pathogens interfere with or exploit the host autophagic pathway for their life-cycle or in order to evade or immune responses. Autophagy is a fundamental eukaryotic cellular process for maintaining homeostasis by degrading cellular proteins, organelles and intracellular pathogens. This process is tightly associated with innate and adaptive immunity.