Evidence map›Paper›PMID 30102389›Full record

Trial reportThe Journal of infectious diseases2019

Subclinical Reactivation of Cytomegalovirus Drives CD4+CD28null T-Cell Expansion and Impaired Immune Response to Pneumococcal Vaccination in Antineutrophil Cytoplasmic Antibody-Associated Vasculitis.

Dimitrios Chanouzas, Michael Sagmeister, Sian Faustini, Peter Nightingale, Alex Richter, Charles J Ferro, Matthew David Morgan, Paul Moss, Lorraine Harper

2 registry-linked trialsOpen access · hybridAbstract readRandomized Controlled Trial
In one paragraph

Trial report in The Journal of infectious diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.2field-weighted citation impact, top 5% 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.

NCT01633476 phase2unknown statusnot on this map

Does CMV Reactivation Cause Functional Impairment of CMV Specific CD4+ T-cells? The Potential for Valaciclovir to Prevent CMV-mediated Adverse Modulation of the Immune System in Patients With ANCA-associated Vasculitis

TypeinterventionalSponsorProfessor Lorraine HarperRan2013 to 2017Enrolled38ConditionsANCA Associated Vasculitis, CMV InfectionArmsValaciclovir
NCT04916704 unknown statusnot on this mapstarted 2022, after this paper: background citation

Subclinical Cytomegalovirus Reactivation in Patients With Newly Diagnosed or Relapsed ANCA-associated Vasculitis and Adverse Clinical Outcomes

TypeobservationalSponsorUniversity Hospital Birmingham NHS Foundation TrustRan2022 to 2025Enrolled70ConditionsANCA Associated Vasculitis
3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Cytomegalovirus and Aging-How Can the Field Move Forward?The Journal of infectious diseases · 2026
    Article
  2. Article
  3. Article
  4. The indirect effects of cytomegalovirus infection-mechanisms and consequences.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. CD4Frontiers in immunology · 2023
    Article
  12. Article
  13. Immunosenescence: an unexplored role in glomerulonephritis.Clinical & translational immunology · 2022
    Review
  14. Article
  15. Functional Changes of T-Cell Subsets with Age and CMV Infection.International journal of molecular sciences · 2021
    Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. ANCA-associated vasculitis.Nature reviews. Disease primers · 2020
    Review
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 2 institutions in 1 country.

Dimitrios ChanouzasInstitute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, United Kingdom.
Michael SagmeisterInstitute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, United Kingdom.
Sian FaustiniInstitute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, United Kingdom.
Peter NightingaleInstitute of Translational Medicine Birmingham, United Kingdom.
Alex RichterInstitute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, United Kingdom.
Charles J FerroDepartment of Nephrology, University Hospitals Birmingham National Health Service Foundation Trust, United Kingdom.
Matthew David MorganDepartment of Nephrology, University Hospitals Birmingham National Health Service Foundation Trust, United Kingdom.
Paul MossInstitute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, United Kingdom.
Lorraine HarperDepartment of Nephrology, University Hospitals Birmingham National Health Service Foundation Trust, United Kingdom.
National Health Service · GBUniversity of Birmingham · GB

Funding

Medical Research Council MR/R011230/1Wellcome TrustWellcome Trust 097962/Z/11/Z
6 · The paper itself

Abstract

Background: Infection is the leading cause of death in antineutrophil cytoplasmic antibody-associated vasculitis (AAV). Expansion of CD4+CD28null T cells is associated with increased risk of infection and mortality, but is only present in cytomegalovirus (CMV)-seropositive individuals. We hypothesized that subclinical CMV reactivation drives CD4+CD28null T-cell expansion, that this is associated with impaired immune response to heterologous antigens, and that antiviral therapy may ameliorate this. Methods: In a proof-of-concept open-label clinical trial, 38 CMV-seropositive AAV patients were randomized to receive valacyclovir for 6 months or no intervention. CMV reactivation was measured monthly in plasma and urine. CD4+CD28null T cells were enumerated at baseline and at 6 months. At 6 months, 36 patients were vaccinated with a 13-valent pneumococcal vaccine. Serotype-specific immunoglobulin G was assayed before and 4 weeks postvaccination to calculate the antibody response ratio. Results: Valacyclovir treatment suppressed subclinical CMV reactivation and reduced CD4+CD28null T-cell proportion. CD4+CD28null T-cell reduction correlated with improved vaccine response, whereas CMV reactivation associated with reduced response to vaccination. Furthermore, expansion of CD4+CD28null T cells was associated with a reduction in the functional capacity of the CD4 compartment. Conclusions: Suppression of CMV may improve the immune response to a T-cell-dependent pneumococcal vaccination in patients with AAV, thus offering potential clinical benefit. Clinical Trials Registration: NCT01633476.

Indexed as

AgedAntibodies, Antineutrophil CytoplasmicAntibodies, ViralAntiviral AgentsCD28 AntigensCD4-Positive T-LymphocytesCytomegalovirusFemaleHumansMaleMiddle AgedPneumococcal InfectionsPneumococcal VaccinesVaccinationValacyclovirVasculitisAntibodies, Antineutrophil CytoplasmicAntibodies, ViralAntiviral AgentsCD28 AntigensPneumococcal VaccinesValacyclovir

Identifiers

PMID30102389
PMCPMC6306020
OpenAlexW2885525933

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.