Evidence map›Paper›PMID 19079794›Full record

ArticleFuture virology2008

Axonal degeneration as a self-destructive defense mechanism against neurotropic virus infection.

Ikuo Tsunoda

Open access · greenAbstract read
In one paragraph

Article in Future virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-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

31 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. SARM1 detection in myelinating glia:Frontiers in cellular neuroscience · 2023
    Article
  4. Article
  5. Article
  6. Lessons from Injury: How Nerve Injury Studies Reveal Basic Biological Mechanisms and Therapeutic Opportunities for Peripheral Nerve Diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Conditional Silencing of H-2DJournal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  11. Review
  12. Cytotoxic CD8Brain pathology (Zurich, Switzerland) · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

1 author at 1 institution in 1 country.

Ikuo TsunodaDepartment of Pathology, Division of Cell Biology & Immunology, University of Utah School of Medicine, 30 North 1900 East, MREB, Room 218, Salt Lake City, Utah 84132, USA.
University of Utah · US

Funding

Axonal degeneration can trigger demyelinating diseaseR21NS059724 · NINDS · UNIVERSITY OF UTAH · PI TSUNODA, IKUO · 2008 to 2009
$357k
NINDS NIH HHS R21 NS059724
6 · The paper itself

Abstract

Theiler's murine encephalomyelitis virus (TMEV) and other neurotropic virus infections result in degeneration of each component of the neuron: apoptosis of the cell body, axonal (Wallerian) degeneration, and dendritic and synaptic pathology. In general, axonal degeneration is detrimental for hosts. However, axonal degeneration can be beneficial in the case of infection with neurotropic viruses that spread in the CNS using axonal transport. C57BL/Wld(S) (Wld(S), Wallerian degeneration slow mutant) mice are protected from axonal degeneration. Wld(S) mice infected with the neurovirulent GDVII strain of TMEV are more resistant to virus infection than wild-type mice, suggesting that axonal preservation contributes to the resistance. By contrast, infection with the less virulent Daniels strain of TMEV results in high levels of virus propagation in the CNS, suggesting that prolonged survival of axons in Wld(S) mice favors virus spread. Thus, axonal degeneration might be a beneficial self-destruct mechanism that limits the spread of neurotropic viruses, in the case of less virulent virus infection. We hypothesize that neurons use 'built-in' self-destruct protection machinery (compartmental neurodegeneration) against neurotropic virus infection, since the CNS is an immunologically privileged site. Early induction of apoptosis in the neuronal cell body limits virus replication. Wallerian degeneration of the axon prevents axonal transport of virus. Dendritic and synaptic degeneration blocks virus transmission at synapses. Thus, the balance between neurodegeneration and virus propagation may be taken into account in the future design of neuroprotective therapy.

Identifiers

PMID19079794
PMCPMC2600527
OpenAlexW2102242769

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.