Get in and get out: Remodeling of the cellular actin cytoskeleton upon HIV‐1 infection

Abstract

The human immunodeficiency virus type 1 (HIV‐1) is an intracellular pathogen whose replication cycle strictly depends on the host cell molecular machinery. HIV‐1 crosses twice the plasma membrane, to get in and to get out of the cell. Therefore, the first and the last line of intracellular component encountered by the virus is the cortical actin network. Here, we review the role of actin and actin‐related proteins in HIV‐1 entry, assembly, budding, and release. We first highlight the mechanisms controlling actin polymerization at the entry site that promote the clustering of HIV‐1 receptors, a crucial step for the virus to fuse with the plasma membrane. Then, we describe how actin is transiently depolymerized locally to allow the capsid to cross the actin cortex, before migrating towards the nucleus. Finally, we review the role of several actin‐binding proteins in actin remodeling events required for membrane deformation and curvature at the viral assembly site as well as for virus release. Strikingly, it appears that common actin‐regulating pathways are involved in viral entry and exit. However, while the role of actin remodeling during entry is well understood, this is not the case during exit. We discuss remaining challenges regarding the actin‐dependent mechanisms involved in HIV‐1 entry and exit, and how they could be overcome.

The role of Vps4 in cancer development

“…Subsequently, it promotes the recruitment and polymerization of critical ESCRT-II and ESCRT-III subunits, leading to the formation of filaments inside the midbody ( 23 ). These filaments, which are associated with the membrane, work in conjunction with the AAA ATPase VPS4 to constrict and cleave the midbody ( 24 , 25 ).…”

Special issue for biology of the cell “intracellular trafficking of viruses”

“…The actin cytoskeleton plays a pivotal role during virus entry, but also exit from cells. The review by Serrano et al describes how HIV-1 remodels the actin cytoskeleton during virus-receptor interactions, and proposes a model for the role of the actin cytoskeleton in HIV-1 assembly, budding, and release (Serrano et al, 2023). Viruses have evolved numerous strategies to travel within the cell from compartment-to-compartment.…”