Evidence map›Paper›PMID 16254349›Full record

ArticleJournal of virology2005

A single amino acid change in rabies virus glycoprotein increases virus spread and enhances virus pathogenicity.

Milosz Faber, Marie-Luise Faber, Amy Papaneri, Michael Bette, Eberhard Weihe, Bernhard Dietzschold, Matthias J Schnell

Open access · greenAbstract 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 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

83 citing papers in PubMed, 190 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Feasibility of Oral Rabies Vaccination of Dogs in Mexico.Tropical medicine and infectious disease · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Negative-Strand RNA Virus-Vectored Vaccines.Methods in molecular biology (Clifton, N.J.) · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

23 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

7 authors at 3 institutions in 2 countries.

Milosz FaberDepartment of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Marie-Luise Faber
Amy Papaneri
Michael Bette
Eberhard Weihe
Bernhard Dietzschold
Matthias J Schnell
Thomas Jefferson University · USMolecular Targeting Technologies (United States) · USPhilipps University of Marburg · DE

Funding

MOLECULAR PATHOGENESIS OF RABIESR01AI045097 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI DIETZSCHOLD, BERNHARD F · 1999 to 2006
$1.6M
Generation of Novel Recombinant Rabies Virus VaccinesR01AI060686 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI DIETZSCHOLD, BERNHARD F · 2005 to 2009
$1.3M
GENERATION OF NOVEL RECOMBINANT RABIES VIRUS VACCINESR56AI060686 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI DIETZSCHOLD, BERNHARD F · 2010 to 2010
$313k
NIAID NIH HHS AI060686NIAID NIH HHS AI45097NIAID NIH HHS R01 AI045097NIAID NIH HHS R01 AI045097-07NIAID NIH HHS R01 AI060686NIAID NIH HHS R01 AI060686-01A1NIAID NIH HHS R56 AI060686
6 · The paper itself

Abstract

Several rabies virus (RV) vaccine strains containing an aspartic acid (Asp) or glutamic acid (Glu) instead of an arginine (Arg) at position 333 of the RV glycoprotein (G) are apathogenic for immunocompetent mice even after intracranial inoculation. However, we previously showed that the nonpathogenic phenotype of the highly attenuated RV strain SPBNGA, which contains a Glu at position 333 of G, is unstable when this virus is passaged in newborn mice. While the Glu(333) remained unchanged after five mouse passages, an Asn(194)-->Lys(194) mutation occurred in RV G. This mutation was associated with increased pathogenicity for adult mice. Using site-directed mutagenesis to exchange Asn(194) with Lys(194) in the G protein of SPBNGA, resulting in SPBNGA-K, we show here that this mutation is solely responsible for the increase in pathogenicity and that the Asn(194)-->Lys(194) mutation does not arise when Asn(194) is exchanged with Ser(194) (SPBNGA-S). Our data presented indicate that the increased pathogenicity of SPBNGA-K is due to increased viral spread in vivo and in vitro, faster internalization of the pathogenic virus into cells, and a shift in the pH threshold for membrane fusion. These results are consistent with the notion that the RV G protein is a major contributor to RV pathogenesis and that the more pathogenic RVs escape the host responses by a faster spread than that of less pathogenic RVs.

Indexed as

Amino Acid SubstitutionAnimalsAntigens, ViralDNA, ComplementaryGlycoproteinsKineticsMiceMutagenesis, Site-DirectedRabiesRabies virusReverse Transcriptase Polymerase Chain ReactionViral Envelope ProteinsAntigens, ViralDNA, Complementaryglycoprotein G, Rabies virusGlycoproteinsViral Envelope Proteins

Identifiers

PMID16254349
PMCPMC1280225
OpenAlexW2096365655

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.