Programmed cell death is an orchestrated biochemical process that leads ultimately to the demise of the cell. Apoptosis is the best characterized form of programmed cell death. Cell changes that have been observed while undergoing apoptosis are chromatin condensation, mitochondria disruption, protease and nuclease activation finally resulting in DNA fragmentation. While necrosis often results in inflammation and adaptive immunity, no inflammatory reaction is associated with apoptosis. Apoptosis is a crucial component for normal multicellular life, playing a key role in development, immunity and the maintenance of homeostasis. There are two main apoptotic pathways: the intrinsic and extrinsic pathways which both lead to caspase (effectors proteolytic enzymes) activation. The extrinsic pathway operates via death receptors on the cell surface, whereas the intrinsic one depends on general metabolic state of cell and mitochondrial membrane integrity. Due to great importance of apoptosis in immunity, many viruses have, as a part of their arsenal, the ability to modulate the apoptotic pathways of the host. It is counter-intuitive that such simple organisms would efficiently affect these most crucial pathways within host, given the relative complexity of the host cells. Yet, viruses have the potential to initiate or inhibit the onset of programmed cell death through the manipulation of a variety key apoptotic proteins. This seminar provides the overview of main viral strategies to inhibit the apoptotic death of the host and thus ensure the infected cell survival for the appropriate length of time in order to propagate and successfully transmit to the next host – from expressing viral Bcl-2 homologues to viral gene products that are able to interfere with cell cycle and oxidative stress regulation, control the transcription of apoptosis-related genes, influence the signaling mediators presentation on the cell surface and caspase activation.