Evidence map›Paper›PMID 37205661›Full record

ArticlePloS one2023

Plasma proteome perturbation for CMV DNAemia in kidney transplantation.

Tara K Sigdel, Patrick Boada, Maggie Kerwin, Priyanka Rashmi, David Gjertson, Maura Rossetti, Swastika Sur, Dane Munar, James Cimino, Richard Ahn and 10 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

20 authors at 3 institutions in 1 country.

Tara K SigdelDepartment of Surgery, University of California San Francisco, San Francisco, CA, United States of America.ORCID 0000-0001-8448-0328
Patrick BoadaDepartment of Surgery, University of California San Francisco, San Francisco, CA, United States of America.
Maggie KerwinDepartment of Surgery, University of California San Francisco, San Francisco, CA, United States of America.
Priyanka RashmiDepartment of Surgery, University of California San Francisco, San Francisco, CA, United States of America.
David GjertsonDepartment of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
Maura RossettiDepartment of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
Swastika SurDepartment of Surgery, University of California San Francisco, San Francisco, CA, United States of America.
Dane MunarDepartment of Surgery, University of California San Francisco, San Francisco, CA, United States of America.
James CiminoDepartment of Surgery, University of California San Francisco, San Francisco, CA, United States of America.
Richard AhnDepartment of Microbiology and Immunology, University of California Los Angeles, Los Angeles, CA, United States of America.
Harry PickeringDepartment of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
Subha SenDepartment of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
Rajesh ParmarDepartment of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.ORCID 0000-0002-6122-4345
Benoit FatouDepartment of Pathology, Harvard Medical School, Boston, MA, United States of America.
Hanno SteenDepartment of Pathology, Harvard Medical School, Boston, MA, United States of America.
Joanna SchaenmanDepartment of Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
Suphamai BunnapradistDepartment of Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
Elaine F ReedDepartment of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
Minnie M SarwalDepartment of Surgery, University of California San Francisco, San Francisco, CA, United States of America.ORCID 0000-0003-1212-3959
CMV Systems Immunobiology Group
University of California, Los Angeles · USUniversity of California, San Francisco · USHarvard University · US

Funding

Project 3: Mapping the Evolution of Chronic Transplant Injury in the Context of CMV InfectionU19AI128913 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LANIER, LEWIS LEE · 2017 to 2021
$11.2M
NIAID NIH HHS U19 AI128913
6 · The paper itself

Abstract

backgroundCytomegalovirus (CMV) infection, either de novo or as reactivation after allotransplantation and chronic immunosuppression, is recognized to cause detrimental alloimmune effects, inclusive of higher susceptibility to graft rejection and substantive impact on chronic graft injury and reduced transplant survival. To obtain further insights into the evolution and pathogenesis of CMV infection in an immunocompromised host we evaluated changes in the circulating host proteome serially, before and after transplantation, and during and after CMV DNA replication (DNAemia), as measured by quantitative polymerase chain reaction (QPCR).

methodsLC-MS-based proteomics was conducted on 168 serially banked plasma samples, from 62 propensity score-matched kidney transplant recipients. Patients were stratified by CMV replication status into 31 with CMV DNAemia and 31 without CMV DNAemia. Patients had blood samples drawn at protocol times of 3- and 12-months post-transplant. Additionally, blood samples were also drawn before and 1 week and 1 month after detection of CMV DNAemia. Plasma proteins were analyzed using an LCMS 8060 triple quadrupole mass spectrometer. Further, public transcriptomic data on time matched PBMCs samples from the same patients was utilized to evaluate integrative pathways. Data analysis was conducted using R and Limma.

resultsSamples were segregated based on their proteomic profiles with respect to their CMV Dnaemia status. A subset of 17 plasma proteins was observed to predict the onset of CMV at 3 months post-transplant enriching platelet degranulation (FDR, 4.83E-06), acute inflammatory response (FDR, 0.0018), blood coagulation (FDR, 0.0018) pathways. An increase in many immune complex proteins were observed at CMV infection. Prior to DNAemia the plasma proteome showed changes in the anti-inflammatory adipokine vaspin (SERPINA12), copper binding protein ceruloplasmin (CP), complement activation (FDR = 0.03), and proteins enriched in the humoral (FDR = 0.01) and innate immune responses (FDR = 0.01).

conclusionPlasma proteomic and transcriptional perturbations impacting humoral and innate immune pathways are observed during CMV infection and provide biomarkers for CMV disease prediction and resolution. Further studies to understand the clinical impact of these pathways can help in the formulation of different types and duration of anti-viral therapies for the management of CMV infection in the immunocompromised host.

Indexed as

Cytomegalovirus InfectionsKidney TransplantationSerpinsCytomegalovirusDNA, ViralHumansProteomeProteomicsDNA, ViralProteomeSERPINA12 protein, humanSerpins

Identifiers

PMID37205661
PMCPMC10198483
OpenAlexW4377116165

What OpenQuestion 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 OpenQuestion graph.