ArticleThe Journal of cell biology2012
Critical role for the kinesin KIF3A in the HIV life cycle in primary human macrophages.
Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- CD4+ T cells facilitate replication of primary HIV-1 strains in macrophages and formation of macrophage internal virus-containing compartments.Journal of virology · 2025Article
- Emerging roles of cytoskeletal transport and scaffold systems in human viral propagation.Animal cells and systems · 2024Review
- Capsid-host interactions for HIV-1 ingress.Microbiology and molecular biology reviews : MMBR · 2023Review
- The two-step cargo recognition mechanism of heterotrimeric kinesin.EMBO reports · 2023Article
- HIV-1 promotes ubiquitination of the amyloidogenic C-terminal fragment of APP to support viral replication.Nature communications · 2023Article
- KIF3A inhibits nasopharyngeal carcinoma proliferation, migration and invasion by interacting with β-catenin to suppress its nuclear accumulation.American journal of cancer research · 2022Article
- Review
- Expression and potential functions of KIF3A/3B to promote nuclear reshaping and tail formation during Larimichthys polyactis spermiogenesis.Development genes and evolution · 2019Article
- Kinesin-2 heterodimerization alters entry into a processive run along the microtubule but not stepping within the run.The Journal of biological chemistry · 2018Article
- Mathematical modeling and quantitative analysis of HIV-1 Gag trafficking and polymerization.PLoS computational biology · 2017Article
- Microtubule Regulation and Function during Virus Infection.Journal of virology · 2017Review
- Myeloid Cell Interaction with HIV: A Complex Relationship.Frontiers in immunology · 2017Review
- Molecular Determinants Directing HIV-1 Gag Assembly to Virus-Containing Compartments in Primary Macrophages.Journal of virology · 2016Article
- siRNA Screen Identifies Trafficking Host Factors that Modulate Alphavirus Infection.PLoS pathogens · 2016Article
- Potent in vitro antiviral activity of Cistus incanus extract against HIV and Filoviruses targets viral envelope proteins.Scientific reports · 2016Article
- Antigen Export Reduces Antigen Presentation and Limits T Cell Control of M. tuberculosis.Cell host & microbe · 2016Article
- Human Immunodeficiency Virus Type 2 (HIV-2) Gag Is Trafficked in an AP-3 and AP-5 Dependent Manner.PloS one · 2016Article
- Extracellular ATP induces the rapid release of HIV-1 from virus containing compartments of human macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- HIV-1 capsids bind and exploit the kinesin-1 adaptor FEZ1 for inward movement to the nucleus.Nature communications · 2015Article
- Sorting of small infectious virus particles by flow virometry reveals distinct infectivity profiles.Nature communications · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are long-lived target cells for HIV infection and are considered viral reservoirs. HIV assembly in macrophages occurs in virus-containing compartments (VCCs) in which virions accumulate and are stored. The regulation of the trafficking and release of these VCCs remains unknown. Using high resolution light and electron microscopy of HIV-1-infected primary human macrophages, we show that the spatial distribution of VCCs depended on the microtubule network and that VCC-limiting membrane was closely associated with KIF3A+ microtubules. Silencing KIF3A strongly decreased virus release from HIV-1-infected macrophages, leading to VCC accumulation intracellularly. Time-lapse microscopy further suggested that VCCs and associated KIF3A move together along microtubules. Importantly, KIF3A does not play a role in HIV release from T cells that do not possess VCCs. These results reveal that HIV-1 requires the molecular motor KIF3 to complete its cycle in primary macrophages. Targeting this step may lead to novel strategies to eliminate this viral reservoir.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.