Abstract
The spread of viral infections can be initiated by the release of cell-free virus particles that infect at a distance or via cell-associated virus, which can promote the direct transmission of viruses between adjacent cells. In the case of human immunodeficiency virus type 1 (HIV-1), cell–cell contact has been found to enhance infection through specialized structures called virological synapses (VS). Cell–cell interactions between virus scavenging dendritic cells and T cells or between infected and uninfected T cells are two major cell interactions that enhance HIV infection. Here we review the features of VS formed between infected and uninfected T cells and focus on how these differ from infection by cell-free virus. While virus particle production is a shared characteristic of both cell-free and cell–cell HIV transmission, cell–cell infection displays several unique features that contribute to the enhanced efficiency of this mode of transmission. Five distinguishing features of HIV spread through T cell virological synapses are discussed below.
Highlights
The spread of viral infections can be initiated by the release of cell-free virus particles that infect at a distance or via cell-associated virus, which can promote the direct transmission of viruses between adjacent cells
virological synapses (VS) formation can be described as a two-part process that begins with adhesion triggered by Env-CD4 interactions and is stabilized by interactions between cellular adhesion molecules (i.e., LFA-1 and ICAM-1,3) [3]
Time-lapse imaging showed that cell adhesion occurred before Gag was recruited to sites of cell–cell contact, indicating that Env functions first as a cell adhesion molecule even before it associates with the newly forming virus particles [2]
Summary
The spread of viral infections can be initiated by the release of cell-free virus particles that infect at a distance or via cell-associated virus, which can promote the direct transmission of viruses between adjacent cells. The T cell VS was initially characterized as an actin-dependent polarization of viral proteins Gag and Env to the site of cell–cell contact on infected donor cells and the recruitment of viral receptor CD4 to the site on uninfected target cells [1]. During cell–cell transmission of HIV-1, an infected T cell first forms a stable adhesive junction with an uninfected CD4+ T cell, which serves as a focal point for de novo viral assembly and transfer [2].
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