Evidence map›Paper›PMID 24894498›Full record

ArticleMucosal immunology2015

Mck2-dependent infection of alveolar macrophages promotes replication of MCMV in nodular inflammatory foci of the neonatal lung.

F R Stahl, K A Keyser, K Heller, Y Bischoff, S Halle, K Wagner, M Messerle, R Förster

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Immune surveillance of cytomegalovirus in tissues.Cellular & molecular immunology · 2024
    Review
  6. Article
  7. Article
  8. Oncolytic α-herpesvirus and myeloid-tropic cytomegalovirus cooperatively enhance systemic antitumor responses.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Murine Cytomegalovirus MCK-2 FacilitatesJournal of virology · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

F R StahlInstitute of Immunology, Hannover Medical School, Hannover, Germany.
K A KeyserInstitute of Virology, Hannover Medical School, Hannover, Germany.
K HellerInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Y BischoffInstitute of Immunology, Hannover Medical School, Hannover, Germany.
S HalleInstitute of Immunology, Hannover Medical School, Hannover, Germany.
K WagnerInstitute of Virology, Hannover Medical School, Hannover, Germany.
M MesserleInstitute of Virology, Hannover Medical School, Hannover, Germany.
R FörsterInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Medizinische Hochschule Hannover · DEUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection with cytomegalovirus (CMV) shows a worldwide high prevalence with only immunocompromised individuals or newborns to become symptomatic. The host's constitution and the pathogen's virulence determine whether disease occurs after infection. Mouse CMV (MCMV) is an appreciated pathogen for in vivo investigation of host-pathogen interactions. It has recently been reported that a single base pair deletion can spontaneously occur in the open reading frame of MCMV-encoded chemokine 2 (MCK2), preventing the expression of the full-length gene product. To study the consequences of this mutation, we compared the Mck2-defective reporter virus MCMV-3D with the newly generated repaired Mck2(+) mutant MCMV-3DR. Compared with MCMV-3D, neonatal mice infected with MCMV-3DR showed severe viral disease after lung infection. Viral disease coincided with high viral activity in multiple organs and increased virus replication in previously described nodular inflammatory foci (NIF) in the lung. Notably, MCMV-3DR showed tropism for alveolar macrophages in vitro and in vivo, whereas MCMV-3D did not infect this cell type. Moreover, in vivo depletion of alveolar macrophages reduced MCMV-3DR replication in the lung. We proposed an Mck2-mediated mechanism by which MCMV exploits alveolar macrophages to increase replication upon first encounter with the host's lung mucosa.

Indexed as

AnimalsAnimals, NewbornCells, CulturedChemokines, CCHerpesviridae InfectionsInflammationLungLung DiseasesMacrophages, AlveolarMiceMice, Inbred C57BLMice, KnockoutMuromegalovirusSequence DeletionSolitary Pulmonary NoduleViral ProteinsChemokines, CCMCK-2 protein, Mouse cytomegalovirus 1Viral Proteins

Identifiers

PMID24894498
OpenAlexW2075713339

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.