Abstract
The virological synapse (VS) is a tight adhesive junction between an HIV-infected cell and an uninfected target cell, across which virus can be efficiently transferred from cell to cell in the absence of cell-cell fusion. The VS has been postulated to resemble, in its morphology, the well-studied immunological synapse (IS). This review article discusses the structural similarities between IS and VS and the shared T cell receptor (TCR) signaling components that are found in the VS. However, the IS and the VS display distinct kinetics in disassembly and intracellular signaling events, possibly leading to different biological outcomes. Hence, HIV-1 exploits molecular components of IS and TCR signaling machinery to trigger unique changes in cellular morphology, migration, and activation that facilitate its transmission and cell-to-cell spread.
Highlights
Many viruses, including HIV-1, HTLV-1 and herpes viruses, disseminate to target cells much more effectively by cell-to-cell transmission as compared to cell-free virion transmission [1,2,3,4,5]
Different types of HIV-1 virological synapse (VS) may be formed between virus-bearing dendritic cells or macrophages and target CD4 T cells [8,9,10,11] and between infected cells and epithelial cells [12,13]
High-resolution microscopy of live CD4 T cells interacting with gp120 and ICAM-1 containing bilayers demonstrated that the VS is initiated by formation of gp120 MCs that coalesce to form a central SMAC (cSMAC)-like structure [51], similar to the T cell receptor (TCR) MCs observed during immunological synapse (IS) assembly [36,37] (Table 1)
Summary
Many viruses, including HIV-1, HTLV-1 and herpes viruses, disseminate to target cells much more effectively by cell-to-cell transmission as compared to cell-free virion transmission [1,2,3,4,5]. It is important to note that in addition to gp120 and its receptors, other membrane proteins, the adhesion molecule LFA-1 and its ligands, the ICAM family, play a significant role in virus-cell interaction These molecules are expressed on HIV-infected cells, target cells and the virus particles themselves [22,23,24,25,26,27]. Regulation of LFA-1 activity through cytoskeleton remodeling and signaling components like PLCγ and ZAP70 modulates the efficiency of HIV-1 entry into activated target T cell [32] These adhesion molecules are found to be recruited to and enriched within HIV-1 VS [2,33]. We will highlight structural and functional similarities and differences between the HIV-1 VS and the IS, and how the specific features of the HIV-1 VS may be beneficial for virus dissemination
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