ArticlePloS one2011
CD4-independent human immunodeficiency virus infection involves participation of endocytosis and cathepsin B.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Review
- Cathepsins in cellular entry of human pathogenic viruses.Journal of virology · 2025Review
- Consequences of HIV infection in the bone marrow niche.Frontiers in immunology · 2023Review
- Unique Mode of Antiviral Action of a Marine Alkaloid against Ebola Virus and SARS-CoV-2.Viruses · 2022Article
- Rlip Protein: A Potential Target for COVID-19.Journal of community hospital internal medicine perspectives · 2022Article
- Cathepsins and Their Endogenous Inhibitors in Host Defense DuringFrontiers in immunology · 2021Review
- Cathepsin B Protease Facilitates Chikungunya Virus Envelope Protein-Mediated Infection via Endocytosis or Macropinocytosis.Viruses · 2020Article
- Data and Text Mining Help Identify Key Proteins Involved in the Molecular Mechanisms Shared by SARS-CoV-2 and HIV-1.Molecules (Basel, Switzerland) · 2020Article
- Ectromelia virus suppresses expression of cathepsins and cystatins in conventional dendritic cells to efficiently execute the replication process.BMC microbiology · 2019Article
- Role of Ezrin Phosphorylation in HIV-1 Replication.Frontiers in microbiology · 2018Article
- Latent human cytomegalovirus enhances HIV-1 infection in CD34Blood advances · 2017Article
- Gamma-interferon-inducible, lysosome/endosome-localized thiolreductase, GILT, has anti-retroviral activity and its expression is counteracted by HIV-1.Oncotarget · 2016Article
- HIV-infected microglia mediate cathepsin B-induced neurotoxicity.Journal of neurovirology · 2015Article
- Antiviral activity of cystatin C against HIV.The Indian journal of medical research · 2015Article
- Fragments of Target Cells are Internalized into Retroviral Envelope Protein-Expressing Cells during Cell-Cell Fusion by Endocytosis.Frontiers in microbiology · 2015Article
- HIV entry: a game of hide-and-fuse?Current opinion in virology · 2014Review
- Interaction of CSFV E2 protein with swine host factors as detected by yeast two-hybrid system.PloS one · 2014Article
- Macrophage derived cystatin B/cathepsin B in HIV replication and neuropathogenesis.Current HIV research · 2014Review
- IFITMs restrict the replication of multiple pathogenic viruses.Journal of molecular biology · 2013Review
- Cathepsin B and cystatin B in HIV-seropositive women are associated with infection and HIV-1-associated neurocognitive disorders.AIDS (London, England) · 2013Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During a comparison of the infectivity of mNDK, a CD4-independent human immunodeficiency virus type 1 (HIV-1) strain, to various cell lines, we found that HeLa cells were much less susceptible than 293T and TE671 cells. Hybridoma cells between HeLa and 293T cells were as susceptible as 293T cells, suggesting that cellular factors enhance the mNDK infection in 293T cells. By screening a cDNA expression library in HeLa cells, cystatin C was isolated as an enhancer of the mNDK infection. Because cathepsin B protease, a natural ligand of cystatin C, was upregulated in HeLa cells, we speculated that the high levels of cathepsin B activities were inhibitory to the CD4-independent infection and that cystatin C enhanced the infection by impairing the excessive cathepsin B activity. Consistent with this idea, pretreatment of HeLa cells with 125 µM of CA-074Me, a cathepsin B inhibitor, resulted in an 8-fold enhancement of the mNDK infectivity. Because cathepsin B is activated by low pH in acidic endosomes, we further examined the potential roles of endosomes in the CD4-independent infection. Suppression of endosome acidification or endocytosis by inhibitors or by an Eps15 dominant negative mutant reduced the infectivity of mNDK in which CD4-dependent infections were not significantly impaired. Taken together, these results suggest that endocytosis, endosomal acidification, and cathepsin B activity are involved in the CD4-independent entry of HIV-1.
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