Evidence map›Paper›PMID 10644358›Full record

ArticleJournal of virology2000

Expanded host cell tropism and cytopathic properties of feline immunodeficiency virus strain PPR subsequent to passage through interleukin-2-independent T cells.

D L Lerner, J H Elder

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-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

23 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Feline models of viral pathogenesis: opportunity knocks.Veterinary journal (London, England : 1997) · 2011
    Article
  6. Article
  7. Feline immunodeficiency virus neuropathogenesis: from cats to calcium.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2007
    Review
  8. Article
  9. Article
  10. Feline immunodeficiency virus targets activated CD4+ T cells by using CD134 as a binding receptor.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  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

2 authors at 1 institution in 1 country.

D L LernerDepartment of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037, USA.
J H Elder
Scripps Research Institute · US

Funding

MOLECULAR CHARACTERIZATION OF FIVR01AI025825 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI ELDER, JOHN H · 1987 to 2015
$6.0M
STRUCTURE AND FUNCTION OF NUCLEOTIDE PHOSPHODIESTERASESR01GM047680 · NIGMS · COLD SPRING HARBOR LABORATORY · PI DAVIS, RONALD L · 1991 to 1994
–
NIAID NIH HHS AI25825NIAID NIH HHS R01 AI025825NIGMS NIH HHS GM47680
6 · The paper itself

Abstract

A cytopathic variant of feline immunodeficiency virus (FIV) strain PPR emerged after passage of wild-type virus on an interleukin-2-independent cell line. The virus, termed FIV-PPRglial, displayed a phenotype markedly different from the parental virus, including the ability to productively infect previously refractory cell lines, induction of large syncytia, and accelerated kinetic properties. A chimeric molecular clone, FIV-PPRchim42, containing the FIV-PPRglial envelope within the backbone of FIV-PPR, exhibited all the characteristics of the FIV-PPRglial phenotype, demonstrating that the viral envelope was responsible for the acquired traits. Subsequent molecular characterization revealed that the FIV-PPRglial envelope contained five amino acid substitutions relative to wild-type FIV-PPR. Mutagenic analyses further demonstrated that the acquired phenotype was minimally attributable to a combination of three mutations, specifically, a glutamine-to-proline change within the second constant domain of the surface protein (SU); a threonine-to-proline change within the V4 loop, also in the SU; and a premature stop codon in the cytoplasmic tail of the transmembrane protein. All three changes were required to produce the FIV-PPRglial phenotype. Cotransfection studies with mutant viruses in combination with each other and with FIV-PPR indicated that the truncated cytoplasmic tail was responsible for the induction of syncytium formation. Receptor usage analyses were pursued, and distinctions were observed between FIV-PPR and FIV-PPRglial. In vitro infections with FIV-PPR, FIV-PPRglial, and FIV-34TF10 on two adherent cell lines were ablated in the presence of SDF1alpha, the natural ligand for CXCR4. In contrast, viral infection of T cells was not limited to CXCR4 usage, and inhibition studies indicate the potential involvement of a CC chemokine receptor.

Indexed as

Amino Acid SequenceAnimalsCatsCell LineChemokine CCL4Chemokine CCL5Cytopathogenic Effect, ViralGiant CellsImmunodeficiency Virus, FelineInterleukin-2Macrophage Inflammatory ProteinsMolecular Sequence DataMutationT-LymphocytesTransfectionTropismChemokine CCL4Chemokine CCL5Interleukin-2Macrophage Inflammatory Proteins

Identifiers

PMID10644358
PMCPMC111663
OpenAlexW2128644514

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.