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Bafilomycin A1 Inhibits HIV-1 Infection by Disrupting Lysosomal Cholesterol Transport.

Byeongwoon Song¹, Olga Korolkova¹

¹Department of Microbiology, Immunology and Physiology, Center for AIDS Health Disparities Research, School of Medicine, Meharry Medical College, Nashville, TN 37208, USA.

|September 28, 2024

Summary

Lysosome-targeting compounds, like bafilomycin A1, inhibit human immunodeficiency virus type 1 (HIV-1) replication by disrupting lysosomal cholesterol transport. This study reveals a novel mechanism impacting HIV-1 post-integration steps.

Keywords:

HIV-1 NPC1 bafilomycin A1 cholesterol transport lysosome

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Area of Science:

Virology
Cell Biology
Biochemistry

Background:

Human immunodeficiency virus type 1 (HIV-1) replication relies on host cell machinery.
The role of lysosomal pathways in HIV-1 replication remains incompletely understood.

Purpose of the Study:

To investigate the impact of lysosome-targeting compounds on HIV-1 replication.
To identify cellular changes associated with HIV-1 inhibition by these compounds.

Main Methods:

Utilized cell culture models of HIV-1 infection.
Treated cells with pharmacological agents inhibiting lysosomal functions, including bafilomycin A1 (a vacuolar ATPase inhibitor).
Analyzed cellular alterations and HIV-1 replication post-treatment.

Main Results:

Lysosome-inhibiting agents, notably bafilomycin A1, significantly interfered with HIV-1 replication, independent of coreceptor tropism.
Bafilomycin A1 treatment disrupted lysosome structure and function, causing cholesterol accumulation and compartment expansion.
Overexpression of Niemann-Pick type C 1 (NPC1) partially reversed bafilomycin A1's inhibitory effect on HIV-1.

Conclusions:

Bafilomycin A1 inhibits HIV-1 replication at post-integration stages, including gene expression, assembly, and/or egress.
Disruption of lysosomal cholesterol trafficking is a key mechanism by which bafilomycin A1 inhibits HIV-1.
Lysosomal pathways represent a potential target for novel anti-HIV-1 therapies.