Evidence map›Paper›PMID 32376620›Full record

ArticleJournal of virology2020

Lactoferrin-Hexon Interactions Mediate CAR-Independent Adenovirus Infection of Human Respiratory Cells.

B David Persson, Annasara Lenman, Lars Frängsmyr, Markus Schmid, Clas Ahlm, Andreas Plückthun, Håvard Jenssen, Niklas Arnberg

Open access · hybridAbstract read
In one paragraph

Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Medical Gas Plasma Inactivates Adenoviruses via Capsid Oxidation.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Construction and application of adenoviral vectors.Molecular therapy. Nucleic acids · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Defensin-driven viral evolution.PLoS pathogens · 2020
    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 3 institutions in 4 countries.

B David PerssonDivision of Virology, Department of Clinical Microbiology, Umeå University, Umeå, Sweden.
Annasara LenmanDivision of Virology, Department of Clinical Microbiology, Umeå University, Umeå, Sweden.
Lars FrängsmyrDivision of Virology, Department of Clinical Microbiology, Umeå University, Umeå, Sweden.
Markus SchmidDepartment of Biochemistry, University of Zurich, Zurich, Switzerland.
Clas AhlmDivision of Virology, Department of Clinical Microbiology, Umeå University, Umeå, Sweden.
Andreas PlückthunDepartment of Biochemistry, University of Zurich, Zurich, Switzerland.
Håvard JenssenDepartment of Science and Environment, Roskilde University, Roskilde, Denmark.
Niklas ArnbergDivision of Virology, Department of Clinical Microbiology, Umeå University, Umeå, Sweden niklas.arnberg@umu.se.
Umeå University · SEUniversity of Zurich · CHRoskilde University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Virus entry into host cells is a complex process that is largely regulated by access to specific cellular receptors. Human adenoviruses (HAdVs) and many other viruses use cell adhesion molecules such as the coxsackievirus and adenovirus receptor (CAR) for attachment to and entry into target cells. These molecules are rarely expressed on the apical side of polarized epithelial cells, which raises the question of how adenoviruses-and other viruses that engage cell adhesion molecules-enter polarized cells from the apical side to initiate infection. We have previously shown that species C HAdVs utilize lactoferrin-a common innate immune component secreted to respiratory mucosa-for infection via unknown mechanisms. Using a series of biochemical, cellular, and molecular biology approaches, we mapped this effect to the proteolytically cleavable, positively charged, N-terminal 49 residues of human lactoferrin (hLF) known as human lactoferricin (hLfcin). Lactoferricin (Lfcin) binds to the hexon protein on the viral capsid and anchors the virus to an unknown receptor structure of target cells, resulting in infection. These findings suggest that HAdVs use distinct cell entry mechanisms at different stages of infection. To initiate infection, entry is likely to occur at the apical side of polarized epithelial cells, largely by means of hLF and hLfcin bridging HAdV capsids via hexons to as-yet-unknown receptors; when infection is established, progeny virions released from the basolateral side enter neighboring cells by means of hLF/hLfcin and CAR in parallel.

Indexed as

A549 CellsAdenoviruses, HumanAdenovirus Infections, HumanCapsid ProteinsEpithelial CellsHumansLactoferrinRespiratory MucosaCapsid Proteinshexon capsid protein, AdenovirusLactoferrinLTF protein, humanadenovirusCARcellular receptorlactoferrintropism

Identifiers

PMID32376620
PMCPMC7343212
OpenAlexW3023087579

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.