Evidence map›Paper›PMID 15681422›Full record

ArticleJournal of virology2005

Kinetics of human immunodeficiency virus type 1 decay following entry into resting CD4+ T cells.

Yan Zhou, Haili Zhang, Janet D Siliciano, Robert F Siliciano

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

130 citing papers in PubMed, 193 citations in OpenAlex.

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  10. Endothelial Cells Promote Productive HIV Infection of Resting CD4AIDS research and human retroviruses · 2022
    Article
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70 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Yan ZhouJohns Hopkins University School of Medicine, 720 Rutland Ave., Baltimore, MD 21205, USA.
Haili Zhang
Janet D Siliciano
Robert F Siliciano
Johns Hopkins University · USHoward Hughes Medical Institute · US

Funding

LATENT VIRAL RESERVOIRS IN HIV1 INFECTIONR01AI043222 · NIAID · JOHNS HOPKINS UNIVERSITY · PI SILICIANO, ROBERT F · 1998 to 2013
$3.5M
NIAID NIH HHS R01 AI043222
6 · The paper itself

Abstract

In untreated human immunodeficiency virus type 1 (HIV-1) infection, most viral genomes in resting CD4(+) T cells are not integrated into host chromosomes. This unintegrated virus provides an inducible latent reservoir because cellular activation permits integration, virus gene expression, and virus production. It remains controversial whether HIV-1 is stable in this preintegration state. Here, we monitored the fate of HIV-1 in resting CD4(+) cells by using a green fluorescent protein (GFP) reporter virus carrying an X4 envelope. After virus entry into resting CD4(+) T cells, both rescuable virus gene expression, visualized with GFP, and rescuable virion production, assessed by p24 release, decayed with a half-life of 2 days. In these cells, reverse transcription goes to completion over 2 to 3 days, and 50% of the viruses that have entered undergo functional decay before reverse transcription is complete. We distinguished two distinct but closely related factors contributing to loss of rescuable virus. First, some host cells undergo virus-induced apoptosis upon viral entry, thereby reducing the amount of rescuable virus. Second, decay processes directly affecting the virus both before and after the completion of reverse transcription contribute to the loss of rescuable virus. The functional half-life of full-length, integration-competent reverse transcripts is only 1 day. We propose that rapid intracellular decay processes compete with early steps in viral replication in infected CD4(+) T cells. Decay processes dominate in resting CD4(+) T cells as a result of the slow kinetics of reverse transcription and blocks at subsequent steps. Therefore, the reservoir of unintegrated HIV-1 in recently infected resting CD4(+) T cells is highly labile.

Indexed as

CD4-Positive T-LymphocytesDNA, ViralHIV-1HIV InfectionsHumansRNA, MessengerTranscription, GeneticVirus IntegrationVirus LatencyDNA, ViralRNA, Messenger

Identifiers

PMID15681422
PMCPMC546571
OpenAlexW2109194095

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.