Formation of these synapses has been shown to involve reorientation of the cytoskeleton, which is triggered by engagement of ICAM-1 on the infected cell's surface and expression of several viral proteins.
By recruiting the receptors and viral particles at the point of contact, these synaptic structures significantly enhance the likelihood of a productive infection.
Viral synapses are thought to explain how cell-to-cell transfer can operate in the HIV infection even when there is a low number of viral particles and a relatively low number of CD4 receptors.
[5][6] Recent study proposes that the primary “killing units” of CD4 T cells leading to CD4 T-cell depletion and progression to AIDS are infected cells (not cell-free viral particles) residing in lymphoid tissues that mediate cell-to-cell spread of the virus via virological synapses.
[7] These findings highlight a previously unappreciated role for the virological synapse in HIV pathogenesis.