Evidence map›Paper›PMID 32143686›Full record

ArticleVirology journal2020

Characterization of HIV-1 uncoating in human microglial cell lines.

Zachary Ingram, Melanie Taylor, Glister Okland, Richard Martin, Amy E Hulme

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  4. HIV-1 capsid shape, orientation, and entropic elasticity regulate translocation into the nuclear pore complex.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  11. Dynactin 1 negatively regulates HIV-1 infection by sequestering the host cofactor CLIP170.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Zachary IngramDepartment of Biomedical Sciences, Missouri State University, Springfield, MO, USA.
Melanie TaylorDepartment of Biomedical Sciences, Missouri State University, Springfield, MO, USA.
Glister OklandDepartment of Biomedical Sciences, Missouri State University, Springfield, MO, USA.
Richard MartinDepartment of Biomedical Sciences, Missouri State University, Springfield, MO, USA.
Amy E HulmeDepartment of Biomedical Sciences, Missouri State University, Springfield, MO, USA. amyhulme@missouristate.edu.
Missouri State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAfter viral fusion with the cell membrane, the conical capsid of HIV-1 disassembles by a process called uncoating. Previously we have utilized the CsA washout assay, in which TRIM-CypA mediated restriction of viral replication is used to detect the state of the viral capsid, to study the kinetics of HIV-1 uncoating in owl monkey kidney (OMK) and HeLa cells. Here we have extended this analysis to the human microglial cell lines CHME3 and C20 to characterize uncoating in a cell type that is a natural target of HIV infection.

methodsThe CsA washout was used to characterize uncoating of wildtype and capsid mutant viruses in CHME3 and C20 cells. Viral fusion assays and nevirapine addition assays were performed to relate the kinetics of viral fusion and reverse transcription to uncoating.

resultsWe found that uncoating initiated within the first hour after viral fusion and was facilitated by reverse transcription in CHME3 and C20 cells. The capsid mutation A92E did not significantly alter uncoating kinetics. Viruses with capsid mutations N74D and E45A decreased the rate of uncoating in CHME3 cells, but did not alter reverse transcription. Interestingly, the second site suppressor capsid mutation R132T was able to rescue the uncoating kinetics of the E45A mutation, despite having a hyperstable capsid.

conclusionsThese results are most similar to previously observed characteristics of uncoating in HeLa cells and support the model in which uncoating is initiated by early steps of reverse transcription in the cytoplasm. A comparison of the uncoating kinetics of CA mutant viruses in OMK and CHME3 cells reveals the importance of cellular factors in the process of uncoating. The E45A/R132T mutant virus specifically suggests that disrupted interactions with cellular factors, rather than capsid stability, is responsible for the delayed uncoating kinetics seen in E45A mutant virus. Future studies aimed at identifying these factors will be important for understanding the process of uncoating and the development of interventions to disrupt this process.

Indexed as

Virus UncoatingAnimalsCapsidCapsid ProteinsCell LineHIV-1HumansKineticsMicrogliaMutationVirus ReplicationCapsid ProteinsCACapsidHIV-1Human immunodeficiency virusMicrogliaUncoating

Identifiers

PMID32143686
PMCPMC7060623
OpenAlexW3011942083

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.