Evidence map›Paper›PMID 30762199›Full record

ReviewVirologica Sinica2019

Manipulating the Interferon Signaling Pathway: Implications for HIV Infection.

Krystelle Nganou-Makamdop, Daniel C Douek

Open access · hybridAbstract readReview
In one paragraph

Review in Virologica Sinica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 17 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

2 authors at 2 institutions in 2 countries.

Krystelle Nganou-MakamdopInstitute of Clinical and Molecular Virology, University Hospital Erlangen, Erlangen, 91054, Germany.
Daniel C DouekHuman Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, 20892, USA. ddouek@mail.nih.gov.ORCID http://orcid.org/0000-0001-5575-8634
National Institutes of Health · USUniversitätsklinikum Erlangen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During human immunodeficiency virus (HIV) infection, type I interferon (IFN-I) signaling induces an antiviral state that includes the production of restriction factors that inhibit virus replication, thereby limiting the infection. As seen in other viral infections, type I IFN can also increase systemic immune activation which, in HIV disease, is one of the strongest predictors of disease progression to acquired immune deficiency syndrome (AIDS) and non-AIDS morbidity and mortality. Moreover, IFN-I is associated with CD4 T cell depletion and attenuation of antigen-specific T cell responses. Therefore, therapeutic manipulation of IFN-I signaling to improve HIV disease outcome is a source of much interest and debate in the field. Recent studies have highlighted the importance of timing (acute vs. chronic infection) and have suggested that specific targeting of type I IFNs and their subtypes may help harness the beneficial roles of the IFN-I system while avoiding its deleterious activities.

Indexed as

Immunity, InnateAnimalsAntiviral AgentsDrug Delivery SystemsHIV InfectionsHumansInflammationInterferon-alphaMiceSignal TransductionSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusVirus ReplicationAntiviral AgentsInterferon-alphaHuman immunodeficiency virus (HIV)InflammationSimian immunodeficiency virus (SIV)Type I interferon (IFN-I)

Identifiers

PMID30762199
PMCPMC6513936
OpenAlexW2914313859

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.