Evidence map›Paper›PMID 11602698›Full record

ArticleJournal of virology2001

Feline Pit2 functions as a receptor for subgroup B feline leukemia viruses.

M M Anderson, A S Lauring, S Robertson, C Dirks, J Overbaugh

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.5field-weighted citation impact, top 46% 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

24 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Convergent evolution of antiviral machinery derived from endogenous retrovirus truncated envelope genes in multiple species.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Immunodeficiencies caused by infectious diseases.The Veterinary clinics of North America. Small animal practice · 2010
    Review
  17. Article
  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

5 authors at 4 institutions in 3 countries.

M M AndersonDivision of Human Biology, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, 98109-1024, USA.
A S Lauring
S Robertson
C Dirks
J Overbaugh
Fred Hutch Cancer Center · USCancer Research Center · USCape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa · ZAInstitut de Biologie Moléculaire et Cellulaire · FR

Funding

VIRAL ONCOLOGYT32CA009229 · NCI · UNIVERSITY OF WASHINGTON · PI LINIAL, MAXINE L · 1985 to 2007
$3.0M
REGULATION OF FELV REPLICATION AND PATHOGENESISR01CA051080 · NCI · UNIVERSITY OF WASHINGTON · PI OVERBAUGH, JULIE M · 1990 to 2004
$1.5M
NCI NIH HHS 2T32 CA09229NCI NIH HHS CA51080NCI NIH HHS R01 CA051080NCI NIH HHS T32 CA009229
6 · The paper itself

Abstract

Different subgroups of feline leukemia virus (FeLV) use different host cell receptors for entry. Subgroup A FeLV (FeLV-A) is the virus that is transmitted from cat to cat, suggesting that cells expressing the FeLV-A receptor are important targets at the earliest stages of infection. FeLV-B evolves from FeLV-A in the infected cat through acquisition of cellular sequences that are related to the FeLV envelope gene. FeLV-Bs have been shown to infect cells using the Pit1 receptor, and some variants can infect cells at a lower efficiency using Pit2. Because these observations were made using receptor proteins of human or rodent origin, the role that Pit1 and Pit2 may play in FeLV-B replication in the cat is unclear. In this study, the feline Pit receptors were cloned and tested for their ability to act as receptors for different FeLV-Bs. Some FeLV-Bs infected cells expressing feline Pit2 and feline Pit1 with equal high efficiency. Variable region A (VRA) in the putative receptor-binding domain (RBD) was a critical determinant for both feline Pit1 and feline Pit2 binding, although other domains in the RBD appear to influence how efficiently the FeLV-B surface unit can bind to feline Pit2 and promote entry via this receptor. An arginine residue at position 73 in VRA was found to be important for envelope binding to feline Pit2 but not feline Pit1. Interestingly, this arginine is not found in endogenous FeLV sequences or in recombinant viruses recovered from feline cells infected with FeLV-A. Thus, while FeLV-Bs that are able to use feline Pit2 can evolve by recombination with endogenous sequences, a subsequent point mutation during reverse transcription may be needed to generate a virus that can efficiently enter the cells using the feline Pit2 as its receptor. These studies suggest that cells expressing the feline Pit2 protein are likely to be targets for FeLV-B infection in the cat.

Indexed as

Amino Acid SequenceAnimalsBiological EvolutionCatsCell LineHumansLeukemia Virus, FelineMolecular Sequence DataReceptors, Virusfeline leukemia virus receptorleukemia virus receptor, gibbon apeReceptors, Virus

Identifiers

PMID11602698
PMCPMC114638
OpenAlexW1974451165

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.