Orchestrated efforts on host network hijacking: Processes governing virus replication

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

Viruses undergo immense variations in their epidemiology and pathogenesis, rendering them difficult to control. For example, HIV is featured by extensive genetic diversity due to its high replication rate and error-prone reverse transcriptase [3] , and influenza viruses have types A to D where type A can be further divided into 18 distinct hemagglutinin and 11 neuraminidase subtypes [4] . Hemagglutinin (HA) and neuraminidase (NA) are the two glycoproteins of the influenza virus membrane that both recognize sialic acids; while HAs bind to sialic acids on carbohydrate side chains of cell surface glycoproteins and glycolipids during the initiation of virus infection, NAs remove sialic acids from infected cell surfaces to allow the release of newly generated viruses to infect more cells [5] . These viral surface glycoproteins undergo antigenic drift that allows for evasion from preexisting humoral immunity [6] . It is therefore of the guiding importance to decipher the primary cellular changes that occur during virus infection with the hope of establishing universal therapeutic strategies targeting viral diseases. The target could be, for example, a panel of pivotal cell signaling players, each controlling one/multiple primary cell process(es) that affect(s) virus replication and having alternatives to maintain normal cell functionalities, or a region where multiple signaling pathways overlap in part of the larger global network.