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

  title={HIV Infection of T Cells: Actin-in and Actin-out},
  author={Yin Liu and Natalya V. Belkina and Stephen Shaw},
  journal={Science Signaling},
  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.

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).

HIV-1 envelope gp 120-induced partial T-cell receptor signaling creates an F-1 actin-depleted zone in the virological synapse 2 3

A model in which the F-actin depleted zone formed within the target CD4 T cell enhances the reception of virions by releasing the physical barrier for HIV-1 entry and facilitating post-entry events is proposed.

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.



Filamin-A regulates actin-dependent clustering of HIV receptors

Human immunodeficiency virus (HIV)-1 infection requires envelope (Env) glycoprotein gp120-induced clustering of CD4 and coreceptors (CCR5 or CXCR4) on the cell surface; this enables Env gp41

Moesin is required for HIV-1-induced CD4-CXCR4 interaction, F-actin redistribution, membrane fusion and viral infection in lymphocytes

It is proposed that activated moesin promotes F-actin redistribution and CD4-CXCR4 clustering and is also required for efficient X4-tropic HIV-1 infection in permissive lymphocytes.

Disruption of the Actin Cytoskeleton Can Complement the Ability of Nef To Enhance Human Immunodeficiency Virus Type 1 Infectivity

The results presented here suggest that Nef functions to allow the HIV genome to penetrate the cortical actin network, a known barrier for intracellular parasitic organisms.

Actin-Dependent Receptor Colocalization Required for Human Immunodeficiency Virus Entry into Host Cells

HIV entry required actin-dependent concentration of coreceptors, which could be disrupted by cytochalasin D (CytoD) without an effect on cell viability or mitosis, but pretreatment of peripheral blood mononuclear cells, but not virus, inhibited entry and infection.

Rac1 Mediates Collapse of Microvilli on Chemokine-Activated T Lymphocytes

The basic residues at the C terminus of Rac1 are critical to Rac1’s participation in ERM dephosphorylation and in microvillar retraction, which elucidate new roles for Rac1 in early signal transduction and cytoskeletal rearrangement of T lymphocytes responding to chemokine.

Retroviral proteins that interact with the host cell cytoskeleton.

Electron Tomography of the Contact between T Cells and SIV/HIV-1: Implications for Viral Entry

The three-dimensional architectures of purified SIV virions in isolation and in contact with CD4+ target cells are determined and the molecular composition and structure of the entry claw may facilitate the identification of improved drugs for the inhibition of HIV-1 entry.

Moesin regulates stable microtubule formation and limits retroviral infection in cultured cells

It is suggested that moesin negatively regulates stable microtubule networks and is a natural determinant of cellular sensitivity to retroviral infection.

Recruitment of HIV and Its Receptors to Dendritic Cell-T Cell Junctions

It is proposed that contact between dendritic cells and T cells facilitates transmission of HIV by locally concentrating virus, receptor, and coreceptor during the formation of an infectious synapse.