HijAkt

Abstract

As obligate parasites of cellular processes, viruses must take over cellular macromolecular machinery. It is also becoming clear that viruses routinely control intracellular signaling pathways through the direct or indirect control of kinases and phosphatases. This control of cellular phosphoproteins is important to promote a variety of viral processes, from control of entry to nuclear function to the stimulation of viral protein synthesis. This review focuses on the takeover of the cellular phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway by a variety of retroviruses, DNA viruses, and RNA viruses, highlighting the functions ascribed to virus activation of PI3K and Akt activity. This review also describes the role that the PI3K/Akt pathway plays in the host response, noting that it that can trigger anti- as well as proviral functions.

ISG15 Regulates Peritoneal Macrophages Functionality against Viral Infection

“…A great number of viruses utilize the PI3K-AKT cell signaling pathway to promote various steps in their replication cycle, such as the regulation of gene expression and the genome replication. Some bacteria and a few non-enveloped viruses also utilize this pathway to trigger their invasion and phagocytosis into cells [41]–[43]. Recently, it has been published that VACV induces AKT phosphorylation to allow viral entry in an integrin β1-dependent manner, suggesting that integrin β1-mediates PI3K/AKT activation induced by VACV [44].…”

Akt Kinase-Mediated Checkpoint of cGAS DNA Sensing Pathway

“…We also determined that the MVA robustly increased IFN-β in phosphorylation-resistant mutant cGAS S291 cells compared to cGAS WT cells. In addition, the PI3K/Akt pathway is activated at the early stage of vaccinia virus infection (Soares et al, 2009) and in some cases, activation of the Akt pathway by viral infection has a central role in viral replication and virus-induced apoptosis (Dunn and Connor, 2012). Therefore, at least some DNA viruses may have evolutionarily adjusted Akt-mediated cGAS regulation for their own needs in viral replication as well as for dampening the host innate immune response.…”

GSK3β and the control of infectious bacterial diseases

“…Thus, targeting of immune signaling molecules by bacteria is an established phenomenon. While it has long been known that multiple viruses, including adenoviruses and influenza viruses, specifically interfere with the PI3K–Akt–GSK3β axis in order to promote replication [66], increasing evidence suggests that one mechanism of immune evasion by bacterial pathogens is to also target GSK3β-related signaling events.…”