Evidence map›Paper›PMID 16014912›Full record

ArticleJournal of virology2005

Frequent coinfection of cells explains functional in vivo complementation between cytomegalovirus variants in the multiply infected host.

Luka Cicin-Sain, Jürgen Podlech, Martin Messerle, Matthias J Reddehase, Ulrich H Koszinowski

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
4.8field-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.

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

72 citing papers in PubMed, 126 citations in OpenAlex.

  1. bTInternational journal of molecular sciences · 2025
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  11. Viral gene drive in herpesviruses.Nature communications · 2020
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  12. Cytomegalovirus inhibition of extrinsic apoptosis determines fitness and resistance to cytotoxic CD8 T cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
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  13. Article
  14. Review
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  19. Quasispecies and virus.European biophysics journal : EBJ · 2018
    Review
  20. Article

12 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Luka Cicin-SainMax von Pettenkofer-Institut, Munich, Germany.
Jürgen Podlech
Martin Messerle
Matthias J Reddehase
Ulrich H Koszinowski
Johannes Gutenberg University Mainz · DELudwig-Maximilians-Universität München · DEMartin Luther University Halle-Wittenberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In contrast to many other virus infections, primary cytomegalovirus (CMV) infection does not fully protect against reinfection. Accordingly, clinical data have revealed a coexistence of multiple human CMV variants/strains in individual patients. Notably, the phenomenon of multiple infection was found to correlate with increased virus load and severity of CMV disease. Although of obvious medical relevance, the mechanism underlying this correlation is unknown. A weak immune response in an individual could be responsible for a more severe disease and for multiple infections. Alternatively, synergistic contributions of variants that differ in their biological properties can lead to qualitative changes in viral fitness by direct interactions such as genetic recombination or functional complementation within coinfected host cells. We have addressed this important question paradigmatically with the murine model by differently designed combinations of two viruses employed for experimental coinfection of mice. Specifically, a murine cytomegalovirus (MCMV) mutant expressing Cre recombinase was combined for coinfection with a mutant carrying Cre-inducible green fluorescent protein gene, and attenuated mutants were combined for coinfection with wild-type virus followed by two-color in situ hybridization studies visualizing the replication of the two viruses in infected host organs. These different approaches concurred in the conclusion that coinfection of host cells is more frequent than statistically predicted and that this coinfection alters virus fitness by functional trans-complementation rather than by genetic recombination. The reported findings make a major contribution to our molecular understanding of enhanced CMV pathogenicity in the multiply infected host.

Indexed as

AnimalsCytomegalovirus InfectionsFemaleGenetic VariationGreen Fluorescent ProteinsIntegrasesLungMiceMice, Inbred BALB CMuromegalovirusNIH 3T3 CellsSpleenViral ProteinsVirulenceCre recombinaseGreen Fluorescent ProteinsIntegrasesViral Proteins

Identifiers

PMID16014912
PMCPMC1181553
OpenAlexW2093760577

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.