Evidence map›Paper›PMID 21734567›Full record

ReviewCurrent opinion in HIV and AIDS2011

Innate immunity in acute HIV-1 infection.

Persephone Borrow

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in HIV and AIDS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.0field-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

33 citing papers in PubMed, 70 citations in OpenAlex.

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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

1 author at 1 institution in 2 countries.

Persephone BorrowNuffield Department of Clinical Medicine, University of Oxford, Oxford, UK. persephone.borrow@ndm.ox.ac.uk
Institute of Molecular Medicine · IN

Funding

Viral Sequencing CoreU19AI067854 · NIAID · DUKE UNIVERSITY · PI LETVIN, NORMAN L · 2006 to 2011
$290.5M
Viral and Host Determinants of HIV-1 TransmissionU01AI067854 · NIAID · DUKE UNIVERSITY · PI HAYNES, BARTON F · 2005 to 2005
$14.9M
NIAID NIH HHS U01 AI067854-06NIAID NIH HHS U19 AI067854
6 · The paper itself

Abstract

purpose of reviewAcute HIV-1 infection (AHI) is composed of the eclipse phase, during which the transmitted virus struggles to avoid eradication and achieve amplification/spread; the expansion phase when virus disseminates and undergoes exponential replication associated with extensive CD4⁺ T-cell destruction; and the containment phase when set-point levels of viremia and immune activation are established. The importance of interactions between HIV-1 and innate responses in determining events throughout AHI is increasingly recognized, and is reviewed here. RECENT

findingsDuring the eclipse phase, HIV-1 subverts dendritic cell functions to promote its replication at mucosal sites and employs multiple strategies to minimize control by type 1 interferons. Systemic virus dissemination is associated with widespread activation of innate responses which fuels HIV-1 replication. To minimize the protective effects of innate responses, HIV-1 resists control by natural killer cells and may impair innate regulation of adaptive responses. Innate responses remain chronically activated after HIV-1 containment which is thought to drive HIV-1 pathogenesis. SUMMARY: Innate responses are pivotal determinants of events at all stages of AHI. Increased understanding of mechanisms involved in innate control of HIV-1 and pathways regulating innate activation during HIV-1 infection could facilitate development of novel approaches to combating this infection.

Indexed as

Immunity, InnateHIV-1HIV InfectionsHumans

Identifiers

PMID21734567
PMCPMC3266478
OpenAlexW2050326976

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.