ArticlePLoS pathogens2005
The cell cycle independence of HIV infections is not determined by known karyophilic viral elements.
Article in PLoS pathogens, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
79 citing papers in PubMed, 120 citations in OpenAlex.
- HIV-based lentiviral vectors: origin and sequence differences.Molecular therapy. Methods & clinical development · 2021Article
- Factors that mold the nuclear landscape of HIV-1 integration.Nucleic acids research · 2021Review
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- The 4th and 112th Residues of Viral Capsid Cooperatively Modulate Capsid-CPSF6 Interactions of HIV-1.AIDS research and human retroviruses · 2020Article
- Multiple Pathways To Avoid Beta Interferon Sensitivity of HIV-1 by Mutations in Capsid.Journal of virology · 2019Article
- The mutation of Transportin 3 gene that causes limb girdle muscular dystrophy 1F induces protection against HIV-1 infection.PLoS pathogens · 2019Article
- CA Mutation N57A Has Distinct Strain-Specific HIV-1 Capsid Uncoating and Infectivity Phenotypes.Journal of virology · 2019Article
- Inhibitors of the integrase-transportin-SR2 interaction block HIV nuclear import.Retrovirology · 2018Article
- The KT Jeang Retrovirology prize 2017: Michael Emerman.Retrovirology · 2017Article
- Roles of Capsid-Interacting Host Factors in Multimodal Inhibition of HIV-1 by PF74.Journal of virology · 2016Article
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- SJP-L-5, a novel small-molecule compound, inhibits HIV-1 infection by blocking viral DNA nuclear entry.BMC microbiology · 2015Article
- Compensatory substitutions in the HIV-1 capsid reduce the fitness cost associated with resistance to a capsid-targeting small-molecule inhibitor.Journal of virology · 2015Article
- The HIV-1 integrase mutant R263A/K264A is 2-fold defective for TRN-SR2 binding and viral nuclear import.The Journal of biological chemistry · 2014Article
- Article
- Inhibiting the HIV integration process: past, present, and the future.Journal of medicinal chemistry · 2014Article
- A cyclophilin homology domain-independent role for Nup358 in HIV-1 infection.PLoS pathogens · 2014Article
- The importance of becoming double-stranded: Innate immunity and the kinetic model of HIV-1 central plus strand synthesis.Virology · 2013Review
19 more citing papers are in PubMed but not listed here.
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Human immunodeficiency virus and other lentiviruses infect cells independent of cell cycle progression, but gammaretroviruses, such as the murine leukemia virus (MLV) require passage of cells through mitosis. This property is thought to be important for the ability of HIV to infect resting CD4+ T cells and terminally differentiated macrophages. Multiple and independent redundant nuclear localization signals encoded by HIV have been hypothesized to facilitate migration of viral genomes into the nucleus. The integrase (IN) protein of HIV is one of the HIV elements that targets to the nucleus; however, its role in nuclear entry of virus genomes has been difficult to describe because mutations in IN are pleiotropic. To investigate the importance of the HIV IN protein for infection of non-dividing cells, and to investigate whether or not IN was redundant with other viral signals for cell cycle-independent nuclear entry, we constructed an HIV-based chimeric virus in which the entire IN protein of HIV was replaced by that of MLV. This chimeric virus with a heterologous IN was infectious at a low level, and was able to integrate in an IN-dependent manner. Furthermore, this virus infected non-dividing cells as well as it infected dividing cells. Moreover, we used the chimeric HIV with MLV IN to further eliminate all of the other described nuclear localization signals from an HIV genome--matrix, IN, Viral Protein R, and the central polypurine tract--and show that no combination of the virally encoded NLS is essential for the ability of HIV to infect non-dividing cells.
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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.