Get in and get out: Remodeling of the cellular actin cytoskeleton upon HIV‐1 infection. (15th February 2023)

• Record Type: Journal Article
• Authors: Serrano, Thomas; Frémont, Stéphane; Echard, Arnaud
• Is Part Of: Biology of the cell. Volume 115:Number 4(2023)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2023-02-15
• Subjects: Actin cytoskeleton -- ESCRT -- HIV‐1 assembly -- HIV‐1 budding -- HIV‐1 entry; Cytology -- Periodicals; Electron microscopy -- Periodicals; 571.6
• DOI: 10.1111/boc.202200085
• Languages: English
• ISSNs: 0248-4900

Abstract

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. Abstract : HIV‐1 closely interacts with the actin cortex underneath the plasma membrane at two crucial steps of its replication cycle: to get in and get out of cells. Here, we review what is currently known about the role of actin and actin‐related proteins in HIV‐1 entry, assembly, budding and release, and discuss the remaining challenges regarding the actin‐dependent mechanisms involved in HIV‐1 entry and exit.