Resolving the Sites of HIV Entry: Dynamin Networks Hold the Key

Abstract

HIV/AIDS pandemic continues to represent a major health concern worldwide and novel strategies are being devised to develop a cure for HIV infection. Central to this is a deeper understanding of host-virus interactions especially at the point of virus entry. HIV can enter target cells either by direct fusion with the plasma membrane or via endocytosis. Herein, we will review the evidence for and against either pathway especially in the context of quiescent CD4 T cells, arguably the most important cellular latent reservoir for HIV. The use of complementary approaches such as single molecule imaging, molecular techniques and small molecule inhibitors have greatly added to our understanding of HIV fusion sites. Cellular GTPase dynamin has emerged as a key player in the process given its ability to modulate HIV infection during virus entry and at later stages of virus replication cycle. These new insights into HIV fusion process in physiologically relevant target cells may in turn be leveraged to advance not only HIV cure efforts, but also immunotherapy.