Antigen presentation and <i>trans</i>-infection of a CD4⁺ T cell mediated by a DC.

<p>Viral binding to distinct cellular receptors allows viral endocytosis via a non-fusogenic mechanism (<b>1</b>). The virus is retained in the multivesicular body compartment (MVB), where it is enriched in tetraspanins such as CD81 and CD63. Part of the virus is degraded in the lysosomes (<b>2</b>), and viral antigens are presented via MHC-II to the T cell receptor (TCR) of CD4⁺ T cells (<b>3</b>) through the formation of an immunological synapse. If an endocytosed virus gains access to the cytoplasm of the DC, it can be processed by the proteasome and crosspresented via MHC-I to CD8⁺ T cells (<b>4</b>). Viral transmission takes place when part of the virus evades classical degradation pathways. MVB recycles back and fuses with the plasma membrane, allowing the liberation of entrapped virus and the productive infection of DC-interacting CD4⁺ T cells (<b>5</b>), a mechanism known as <i>trans</i>-infection. The contact area between an uninfected DC bearing HIV infectious particles and a CD4⁺ T cell is termed the infectious synapse.