<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Song B</submitter><funding>NCRR NIH HHS</funding><funding>NIMHD NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>1374</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11435809</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(9)</volume><pubmed_abstract>The productive replication of human immunodeficiency virus type 1 (HIV-1) involves intricate interactions between viral proteins and host cell machinery. However, the contributions of the lysosomal pathways for HIV-1 replication are not fully understood. The goal of this study was to determine the impact of lysosome-targeting compounds on HIV-1 replication and identify the cellular changes that are linked to HIV-1 inhibition using cell culture models of HIV-1 infection. Here, we demonstrate that the treatment of cells with various pharmacological agents known to inhibit lysosomal functions interfere with HIV-1 replication. The vacuolar ATPase (V-ATPase) inhibitor bafilomycin A1 exerted a potent inhibition of HIV-1 replication. Bafilomycin A1 inhibition of HIV-1 was independent of corecepto</pubmed_abstract><journal>Viruses</journal><pubmed_title>Bafilomycin A1 Inhibits HIV-1 Infection by Disrupting Lysosomal Cholesterol Transport.</pubmed_title><pmcid>PMC11435809</pmcid><funding_grant_id>U54 CA163069</funding_grant_id><funding_grant_id>U54 MD007586</funding_grant_id><funding_grant_id>S10 RR025497</funding_grant_id><pubmed_authors>Song B</pubmed_authors><pubmed_authors>Korolkova O</pubmed_authors></additional><is_claimable>false</is_claimable><name>Bafilomycin A1 Inhibits HIV-1 Infection by Disrupting Lysosomal Cholesterol Transport.</name><description>The productive replication of human immunodeficiency virus type 1 (HIV-1) involves intricate interactions between viral proteins and host cell machinery. However, the contributions of the lysosomal pathways for HIV-1 replication are not fully understood. The goal of this study was to determine the impact of lysosome-targeting compounds on HIV-1 replication and identify the cellular changes that are linked to HIV-1 inhibition using cell culture models of HIV-1 infection. Here, we demonstrate that the treatment of cells with various pharmacological agents known to inhibit lysosomal functions interfere with HIV-1 replication. The vacuolar ATPase (V-ATPase) inhibitor bafilomycin A1 exerted a potent inhibition of HIV-1 replication. Bafilomycin A1 inhibition of HIV-1 was independent of corecepto</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Aug</publication><modification>2026-07-09T11:11:00.336Z</modification><creation>2025-04-04T23:41:46.691Z</creation></dates><accession>S-EPMC11435809</accession><cross_references><pubmed>39339852</pubmed><doi>10.3390/v16091374</doi></cross_references></HashMap>