Evidence map›Paper›PMID 31055732›Full record

ReviewCurrent HIV/AIDS reports2019

Pathogenic Role of Type I Interferons in HIV-Induced Immune Impairments in Humanized Mice.

Lishan Su

Open access · greenAbstract readReview
In one paragraph

Review in Current HIV/AIDS reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Targeting the pDC/IFN-I axis in HIV-1 immunotherapy.Current opinion in HIV and AIDS · 2026
    Review
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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 1 country.

Lishan SuDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. lsu@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

Blocking type I interferon signaling to reverse T cell exhaustion and control HIV-1 reservoirsR01AI136990 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI AMARA, RAMA RAO, BOSINGER, STEVEN EDWARD · 2018 to 2022
$4.2M
Modeling immune impairments and pathogenesis in novel humanized mice for HBV-HIV co-infectionR01AI138797 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PLOSS, ALEXANDER, SU, LISHAN · 2018 to 2022
$3.9M
HIV-1 Vpr disrupts the IFN-TET-ISG pathway to promote HIV-1 infection and persistenceR01AI127346 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2016 to 2020
$2.7M
Immune Mechanisms of Elevated Liver Diseases During HIV InfectionR01DK119937 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2018 to 2022
$1.9M
NIAID NIH HHS R01 AI127346NIAID NIH HHS R01 AI136990NIAID NIH HHS R01 AI138797NIDDK NIH HHS R01 DK119937
6 · The paper itself

Abstract

purpose of reviewRecent findings on the critical pathogenic role of type 1 interferons (IFN-I) in HIV-1 persistence in humanized mice suggest that inhibiting IFN-I signaling transiently will reverse HIV-induced inflammatory diseases and rescue anti-HIV immunity to control HIV-1 reservoirs. RECENT

findingsIn both humanized mice and in monkeys, IFN-I signaling is functionally defined to play an important role in suppressing early HIV-1 and SIV infection. During persistent infection in humanized mice, however, IFN-I signaling is revealed to induce T cell depletion and impairment. Interestingly, in HIV-infected mice with effective combination antiretroviral therapy (cART), blocking IFN-I signaling reverses HIV-induced inflammation, rescues anti-HIV T cells, and reduces HIV-1 reservoirs. These findings functionally define the role of IFN-I in HIV-1 reservoir persistence and suggest that blocking IFN-I signaling will provide a novel therapeutic strategy to (i) reverse inflammation-associated diseases in HIV patients under cART, (ii) rescue host anti-HIV immunity, and (iii) reduce or control HIV-1 reservoirs.

Indexed as

AnimalsAnti-Retroviral AgentsHIV-1HIV InfectionsHumansInterferon Type IMiceSignal TransductionT-LymphocytesAnti-Retroviral AgentsInterferon Type IHIV-1 reservoirsIFNARInflammationISGpDCT cell exhaustion

Identifiers

PMID31055732
PMCPMC6579639
OpenAlexW2944661973

What OpenQuestion holds

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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.