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HijAkt: The PI3K/Akt pathway in virus replication and pathogenesis
1Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts, USA.
Progress in Molecular Biology and Translational Science
|February 21, 2012
Summary
Viruses hijack host cell machinery, particularly the phosphatidylinositol-3-kinase (PI3K)/Akt pathway, to control viral replication. This pathway
Area of Science:
- Virology
- Cellular Biology
- Molecular Biology
Background:
- Viruses are obligate intracellular parasites that manipulate host cell machinery.
- Viruses frequently control host intracellular signaling pathways, including those involving kinases and phosphatases.
- Phosphoprotein regulation is crucial for various viral life cycle stages, from entry to protein synthesis.
Purpose of the Study:
- To review the takeover of the phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway by diverse viruses.
- To highlight the functions of PI3K/Akt pathway activation by viruses.
- To describe the dual role of the PI3K/Akt pathway in host antiviral and proviral responses.
Main Methods:
- Literature review of viral manipulation of host signaling pathways.
- Focus on the PI3K/Akt signaling cascade.
- Analysis of viral and host factors influencing PI3K/Akt activity.
Main Results:
- Various viruses (retroviruses, DNA viruses, RNA viruses) activate the PI3K/Akt pathway.
- Activated PI3K/Akt signaling contributes to viral entry, nuclear functions, and protein synthesis.
- The PI3K/Akt pathway can elicit both anti-viral and pro-viral host responses.
Conclusions:
- Viral exploitation of the PI3K/Akt pathway is a common strategy for replication.
- Understanding PI3K/Akt modulation by viruses is key to deciphering host-pathogen interactions.
- The PI3K/Akt pathway represents a critical nexus of viral manipulation and host defense.
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