Evidence map›Paper›PMID 19741482›Full record

ArticleAIDS (London, England)2009

HIV-1 infection of macrophages is dependent on evasion of innate immune cellular activation.

Jhen Tsang, Benjamin M Chain, Robert F Miller, Benjamin L J Webb, Wendy Barclay, Greg J Towers, David R Katz, Mahdad Noursadeghi

Abstract read
In one paragraph

Article in AIDS (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Meta-Analysis ofFrontiers in immunology · 2019
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1 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

8 authors at 2 institutions in 2 countries.

Jhen TsangDivision of Infection and Immunity, University College London, London, UK.
Benjamin M Chain
Robert F Miller
Benjamin L J Webb
Wendy Barclay
Greg J Towers
David R Katz
Mahdad Noursadeghi
Institute of Infection and Immunity · CAUniversity College London · GB

Funding

Medical Research Council G0801172Medical Research Council G0801172(87743)Medical Research Council G0900950Medical Research Council G9721629Wellcome Trust 076608Wellcome Trust 077161
6 · The paper itself

Abstract

objectiveThe cellular innate immune response to HIV-1 is poorly characterized. In view of HIV-1 tropism for macrophages, which can be activated via pattern recognition receptors to trigger antimicrobial defences, we investigated innate immune responses to HIV-1 by monocyte-derived macrophages.

designIn a model of productive HIV-1 infection, cellular innate immune responses to HIV-1 were investigated, at the level of transcription factor activation, specific gene expression and genome-wide transcriptional profiling. In addition, the viral determinants of macrophage responses and the physiological effect of innate immune cellular activation on HIV-1 replication were assessed.

resultsProductive HIV-1 infection did not activate nuclear factor-kappaB and interferon regulatory factor 3 transcription factors or interferon gene expression (IFN) and caused remarkably small changes to the host-cell transcriptome, with no evidence of inflammatory or IFN signatures. Evasion of IFN induction was not dependent on HIV-1 envelope-mediated cellular entry, inhibition by accessory proteins or reverse transcription of ssRNA that may reduce innate immune cellular activation by viral RNA. Furthermore, IFNbeta priming did not sensitize responses to HIV-1. Importantly, exogenous IFNbeta or stimulation with the RNA analogue poly I:C to simulate innate immune activation invoked HIV-1 restriction.

conclusionWe conclude that macrophages lack functional pattern recognition receptors for this virus and that HIV-1 tropism for macrophages helps to establish a foothold in the host without triggering innate immune cellular activation, which would otherwise block viral infection effectively.

Indexed as

Cells, CulturedGene Expression Regulation, ViralHIV-1HIV InfectionsHumansImmune EvasionImmunity, CellularImmunity, InnateMacrophage ActivationMacrophagesNF-kappa BSignal TransductionViral TropismVirus ReplicationNF-kappa B

Identifiers

PMID19741482
PMCPMC2873676
OpenAlexW2169496824

What OpenQuestion holds

Textmetadata
LicenceTDM
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.