How HIV Takes Advantage of the Cytoskeleton in Entry and Replication
2011
How HIV Exploits the Cytoskeleton for Entry and Replication
publication
Evidence: moderate
Author Information
Author(s): Bettina Stolp, Oliver T. Fackler
Primary Institution: Department of Infectious Diseases, Virology, University Hospital Heidelberg
Hypothesis
HIV-1 has evolved strategies to exploit and modulate the actin cytoskeleton for its purposes.
Conclusion
HIV-1 takes advantage of the cellular cytoskeleton at various steps in its replication cycle, particularly during the entry process.
Supporting Evidence
- HIV-1 exploits the actin cytoskeleton for efficient entry into host cells.
- The Nef protein plays a significant role in modulating actin dynamics.
- HIV-1 can prime uninfected cells for future infection by manipulating the cytoskeleton.
Takeaway
HIV-1 uses the cell's skeleton to help it get inside and move around, making it easier for the virus to spread.
Methodology
This review summarizes recent findings on HIV-1's interaction with the host cell cytoskeleton.
Limitations
Knowledge is limited at other steps of the replication cycle.
Digital Object Identifier (DOI)
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