Evidence map›Paper›PMID 29272392›Full record

ArticleClinical infectious diseases : an official publication of the Infectious Diseases Society of America2018

Pegylated Interferon-α-Induced Natural Killer Cell Activation Is Associated With Human Immunodeficiency Virus-1 DNA Decline in Antiretroviral Therapy-Treated HIV-1/Hepatitis C Virus-Coinfected Patients.

Stéphane Hua, Selena Vigano, Samantha Tse, Ouyang Zhengyu, Sean Harrington, Jordi Negron, Pilar Garcia-Broncano, Giulia Marchetti, Miguel Genebat, Manuel Leal and 4 more

Open access · greenAbstract read
In one paragraph

Article in Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 40 citations in OpenAlex.

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  12. Engaging innate immunity in HIV-1 cure strategies.Nature reviews. Immunology · 2022
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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

14 authors at 6 institutions in 3 countries.

Stéphane HuaRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Selena ViganoRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Samantha TseRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Ouyang ZhengyuRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Sean HarringtonRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Jordi NegronRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Pilar Garcia-BroncanoRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Giulia MarchettiDepartment of Health Sciences, Clinic of Infectious and Tropical Diseases, San Paolo Hospital, University of Milan, Italy.
Miguel GenebatLaboratory of Immunovirology, University of Seville, Spain.
Manuel LealLaboratory of Immunovirology, University of Seville, Spain.
Salvador ResinoUnit of Viral Infection and Immunity, National Center for Microbiology, Institute of Health Carlos III, Majadahonda, Madrid, Spain.
Ezequiel Ruiz-MateosLaboratory of Immunovirology, University of Seville, Spain.
Mathias LichterfeldRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Xu G YuRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard, Cambridge.
Ragon Institute of MGH, MIT and Harvard · USInstituto de Salud Carlos III · ESUniversidad de Sevilla · ESBrigham and Women's Hospital · USHospital Universitario Virgen del Rocío · ESUniversity of Milan · IT

Funding

Immunoregulatory Function of Myelomonocytic Receptors in HIV-1 InfectionR01AI078799 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI YU, XU · 2008 to 2017
$4.1M
A systems biology approach to fingerprint HIV immune defense in Elite ControllersR01HL134539 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI YU, XU · 2016 to 2019
$3.3M
Targeting HIV-1 persistence with Interferon-aR33AI116228 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI YU, XU · 2016 to 2018
$1.5M
Viral and Immune Determinants of HIV ReboundR56AI125109 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI LI, JONATHAN · 2016 to 2016
$897k
Targeting HIV-1 persistence with Interferon-aR21AI116228 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI YU, XU · 2014 to 2015
$479k
NHLBI NIH HHS R01 HL134539NIAID NIH HHS R01 AI078799NIAID NIH HHS R21 AI116228NIAID NIH HHS R33 AI116228NIAID NIH HHS R56 AI125109
6 · The paper itself

Abstract

Background: Interferon alpha (IFN-α) can potently reduce human immunodeficiency virus type 1 (HIV-1) replication in tissue culture and animal models, but may also modulate residual viral reservoirs that persist despite suppressive antiretroviral combination therapy. However, mechanisms leading to viral reservoir reduction during IFN-α treatment are unclear. Methods: We analyzed HIV-1 gag DNA levels in CD4 T cells by digital droplet polymerase chain reaction and CD8 T-cell and natural killer (NK) cell phenotypes by flow cytometry in a cohort of antiretroviral therapy-treated HIV-1/hepatitis C virus-coinfected patients (n = 67) undergoing treatment for hepatitis C infection with pegylated IFN-α and ribavirin for an average of 11 months. Results: We observed that IFN-α treatment induced a significant decrease in CD4 T-cell counts (P < .0001), in CD4 T-cell-associated HIV-1 DNA copies (P = .002) and in HIV-1 DNA copies per microliter of blood (P < .0001) in our study patients. Notably, HIV-1 DNA levels were unrelated to HIV-1-specific CD8 T-cell responses. In contrast, proportions of total NK cells, CD56brightCD16- NK cells, and CD56brightCD16+ NK cells were significantly correlated with reduced levels of CD4 T-cell-associated HIV-1 DNA during IFN-α treatment, especially when coexpressing the activation markers NKG2D and NKp30. Conclusions: These data suggest that the reduction of viral reservoir cells during treatment with IFN-α is primarily attributable to antiviral activities of NK cells.

Indexed as

AdultAgedAntiretroviral Therapy, Highly ActiveCohort StudiesCoinfectionDisease ReservoirsDNA, ViralFemalegag Gene Products, Human Immunodeficiency VirusHepacivirusHepatitis CHIV-1HIV InfectionsHumansInterferon-alphaKiller Cells, NaturalDNA, Viralgag Gene Products, Human Immunodeficiency VirusInterferon-alphapeginterferon alfa-2aPolyethylene GlycolsRecombinant ProteinsRibavirin

Identifiers

PMID29272392
PMCPMC5982807
OpenAlexW2778455165

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.