Abstract

Classically viruses are released from cells as infectious particles which then diffuse in three dimensions through the fluid phase until they contact a permissive cell. Although a good strategy for long-distance viral spread within or between hosts, this is generally not an efficient infection mechanism.

A faster way to disseminate is via direct viral spread between contacting cells. Retroviruses infect leukocytes that have no inbuilt polarity and are not stably associated with other cells. In order to spread by contact-dependent mechanisms, they either have to induce cell-cell contact or opportunistically move between cells when they form contacts during their normal physiological function.

One such opportunity arises when cells form immunological synapses, and retroviruses appear to hijack this process to form what we and others have termed “virological synapses”.

Another mode of spread takes place when retrovirally-infected cells are phagocytosed by macrophages, resulting in highly efficient macrophage infection.

In this presentation I will discuss how we think HIV -1 moves between cells of the immune system and how this may affect viral pathogenesis.