Evidence map›Paper›PMID 35435733›Full record

ArticlemBio2022

Plasma CD16

Erika G Marques de Menezes, Xutao Deng, Jocelyn Liu, Scott A Bowler, Cecilia M Shikuma, Mars Stone, Peter W Hunt, Lishomwa C Ndhlovu, Philip J Norris

Open access · goldAbstract read
In one paragraph

Article in mBio, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.6field-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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. CD27Frontiers in immunology · 2023
    Article
  10. Article
  11. Article
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

9 authors at 4 institutions in 1 country.

Erika G Marques de MenezesVitalant Research Institute, San Francisco, California, USA.ORCID 0000-0002-3273-6755
Xutao DengVitalant Research Institute, San Francisco, California, USA.
Jocelyn LiuDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicinegrid.471410.7, New York, New York, USA.
Scott A BowlerDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicinegrid.471410.7, New York, New York, USA.
Cecilia M ShikumaDepartment of Tropical Medicine, University of Hawaii, Honolulu, Hawaii, USA.
Mars StoneVitalant Research Institute, San Francisco, California, USA.
Peter W HuntDepartment of Medicine, UCSF, San Francisco, California, USA.
Lishomwa C Ndhlovu *Division of Infectious Diseases, Department of Medicine, Weill Cornell Medicinegrid.471410.7, New York, New York, USA.
Philip J Norris *Vitalant Research Institute, San Francisco, California, USA.
University of California, San Francisco · USCornell University · USUniversity of Hawaiʻi at Mānoa · USUniversity of Hawaii System · US

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEVEN Grant DEEKS · 1988 to 2026
$93.6M
Tracking and Evaluation CoreU54GM138062 · NIGMS · UNIVERSITY OF HAWAII AT MANOA · PI SHIKUMA, CECILIA M. · 2021 to 2025
$15.5M
Impact of Treating Asymptomatic CMV Replication on Cardiovascular Risk in Treated HIV InfectionR01HL152957 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PETER W HUNT, Priscilla Y. Hsue · 2020 to 2026
$3.7M
Persistent Functional Immune Defects in Treated HIV InfectionK24AI145806 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUNT, PETER W · 2020 to 2024
$921k
NHLBI NIH HHS R01 HL152957NIAID NIH HHS K24 AI145806NIAID NIH HHS P30 AI027763NIGMS NIH HHS U54 GM138062
6 · The paper itself

Abstract

HIV-infected individuals have increased risk for cardiovascular disease (CVD) despite suppressive antiretroviral therapy (ART). This is likely a result of persistent immune activation and systemic inflammation. Extracellular vesicles (EVs) have emerged as critical mediators of intercellular communication and may drive inflammation contributing to CVD. EVs were characterized in plasma from 74 HIV-infected individuals on combination antiretroviral therapy (cART) and 64 HIV-uninfected controls with paired carotid intima-media thickness (cIMT) assessment. EVs were profiled with markers reflecting lymphoid, myeloid, and endothelial origin. Seventeen plasma inflammatory biomarkers were also assessed. Human umbilical vein endothelial cell (HUVEC) apoptosis was quantified after EV exposure. A significant correlation was observed in HIV-infected participants between cIMT and EVs expressing CD16, and the monocyte-related markers CD4, CD14, and CX3CR1 showed a similar but nonsignificant association with cIMT. No significant correlation between cIMT measurements from HIV-uninfected individuals and EVs was observed. Levels of serum amyloid A, C-reactive protein, and myeloperoxidase significantly correlated with CD14

Indexed as

Cardiovascular DiseasesExtracellular VesiclesHIV InfectionsAdultAntiretroviral Therapy, Highly ActiveBiomarkersCarotid ArteriesCarotid Intima-Media ThicknessGPI-Linked ProteinsHumansInflammationReceptors, IgGRisk FactorsBiomarkersFCGR3B protein, humanGPI-Linked ProteinsReceptors, IgGapoptosiscardiovascular diseasecarotid intima-mediaendothelial cellsextracellular vesicleshuman immunodeficiency virusmonocytes

Identifiers

PMID35435733
PMCPMC9239192
OpenAlexW4223901686

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.