HIV Infection of T Cells: Actin-in and Actin-out

@article{Liu2009HIVIO,
  title={HIV Infection of T Cells: Actin-in and Actin-out},
  author={Yin Liu and Natalya V. Belkina and Stephen Shaw},
  journal={Science Signaling},
  year={2009},
  volume={2},
  pages={pe23 - pe23}
}
The coordinated activities of various actin-binding proteins facilitate entry of HIV into T cells. Three studies shed light on the decade-old observation that the actin cytoskeleton is hijacked to facilitate entry of HIV into its target cells. Polymerization of actin is required to assemble high concentrations of CD4 and CXCR4 at the plasma membrane, which promote viral binding and entry in both the simple model of infection by free virus and the more physiologically relevant route of infection… 

The trinity of the cortical actin in the initiation of HIV-1 infection

The purpose of this review is to examine, in detail, the manifestation of viral dependence on the actin cytoskeleton, and present a model of how HIV utilizes actin dynamics to initiate infection.

Actin-binding Protein Drebrin Regulates HIV-1-triggered Actin Polymerization and Viral Infection*

The role of the actin modulator drebrin is established as a negative regulator of HIV entry and HIV-mediated cell fusion by modulating viral entry, mainly through the control of actin cytoskeleton polymerization in response to HIV-1.

LIM Kinase 1 Modulates Cortical Actin and CXCR4 Cycling and Is Activated by HIV-1 to Initiate Viral Infection*

HIV hijacks LIMK to control the cortical actin dynamics for the initiation of viral infection of CD4 T cells, suggesting that HIV-mediated early actin polymerization may directly regulate the CXCR4 receptor during viral entry and is involved in viral DNA synthesis.

Gelsolin activity controls efficient early HIV-1 infection

Gelsolin is a new factor that can limit HIV-1 infection acting at a pre-fusion step, and accordingly, cell-signals that regulate gelsolin expression and/or its actin-severing activity may be crucial to combat HIV- 1 infection.

Quantitative Analysis of the Processes and Signaling Events Involved in Early HIV-1 Infection of T Cells

This model shows that moesin activation is induced by virus signaling, while filamin-A is mobilized by the receptor capping, and gelsolin inhibition is seen as a promising target for preventing HIV-1 entry into lymphocytes, due to its role in facilitating the capping needed for the invasion.

Plasma membrane signaling in HIV-1 infection.

All-Round Manipulation of the Actin Cytoskeleton by HIV

It is reviewed how the virus uses different strategies to manipulate cellular actin networks and increase the efficiency of various stages of its life cycle and how their coordinated deregulation can lead to changes in cellular behavior that promote viral spreading.

Actin dynamics at the immunological synapse

A perspective on the roles played by actin regulator molecules during the formation of the immunological synapse (IS) which is defined as the structure formed by the interaction between lymphocytes and antigen-presenting cells (APC).

Chemokine Coreceptor Signaling in HIV-1 Infection and Pathogenesis

It is likely that virus-mediated signaling events may facilitate infection in various immunologic settings in vivo where cellular conditions need to be primed and HIV may exploit the chemokine signaling network shared among immune cells to gain access to downstream cellular components, which can then serve as effective tools to break cellular barriers.
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