Orchestrated efforts on host network hijacking: Processes governing virus replication

Dai, Xiaofeng; Hakizimana, Olivier; Zhang, Xuanhao; Kaushik, Aman Chandra; Zhang, Jianying

Cell survival programs are the outcome of the collective efforts of cell defense and cell physiology adaptations. Immune response stimulates autophagy by PRRs via autophagic adaptors to eradicate intracellular microorganisms [148] . Interferon, the crucial mediators of innate immune response, induces apoptosis of virusinfected cells and cellular resistance to viral infection [149] . Cell cycle arrest can provoke signals to induce apoptosis, where fatty acids such as butyrate are the pivotal molecules attracting cells in the arrested states [150] . Retroviruses, in particular, set cells to transient cell cycle arrest during its amalgamation into the host genome to activate enzymes necessary for DNA repair, and failed recombination lead to apoptosis [151] . Cell cycle arrest and DNA damage can trigger autophagy in response to cytoplasmic signals [152] . Lipids such as short-chain fatty acids (mostly propionate and butyrate) could induce autophagy [153] and/or apoptosis [154] , as substantiated in colon cancer cells.