HIV-1 diverts cortical actin for particle assembly and release

Area of Science:

• Virology
• Cell Biology
• Immunology

Background:

• Enveloped viruses, including HIV-1, bud from host cell membranes.
• The precise role of cortical actin in viral assembly and budding has been debated.
• Understanding these processes is crucial for developing antiviral strategies.

Purpose of the Study:

• To investigate the role of cortical actin in Human Immunodeficiency Virus type 1 (HIV-1) assembly and particle release.
• To determine if HIV-1 Gag protein assembly is influenced by the density of cortical actin.
• To explore the potential involvement of host factors in modulating actin dynamics during viral assembly.

Main Methods:

• Assessing HIV-1 particle release and Gag assembly clusters in infected CD4 T lymphocytes.
• Utilizing in vitro quantitative model systems to study HIV-1 Gag protein behavior.
• Investigating the recruitment and association of the host factor Arpin with viral Gag protein at the cell membrane.

Main Results:

• Preventing actin branching significantly increased HIV-1 particle release and Gag assembly clusters.
• HIV-1 Gag protein preferentially assembled in F-actin-deficient areas of the T cell plasma membrane.
• The host factor Arpin was recruited to the membrane of infected T cells and associated with HIV-1 Gag.

Conclusions:

• HIV-1 assembly and particle release are favored in regions with low cortical actin density.
• HIV-1 may actively promote viral assembly by subverting Arpin to induce local actin debranching.
• These findings offer new insights into the mechanisms of HIV-1 replication and potential therapeutic targets.