Identification of a cellular cofactor required for infection by feline leukemia virus

Science. 2000 Mar 10;287(5459):1828-30. doi: 10.1126/science.287.5459.1828.


Retroviral infection involves continued genetic variation, leading to phenotypic and immunological selection for more fit virus variants in the host. For retroviruses that cause immunodeficiency, pathogenesis is linked to the emergence of T cell-tropic, cytopathic viruses. Here we show that an immunodeficiency-inducing, T cell-tropic feline leukemia virus (FeLV) has evolved such that it cannot infect cells unless both a classic multiple membrane-spanning receptor molecule (Pit1) and a second coreceptor or entry factor are present. This second receptor component, which we call FeLIX, was identified as an endogenously expressed protein that is similar to a portion of the FeLV envelope protein. This cellular protein can function either as a transmembrane protein or as a soluble component to facilitate infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cats
  • Cell Line
  • Cloning, Molecular
  • Dogs
  • Evolution, Molecular
  • Leukemia Virus, Feline / genetics
  • Leukemia Virus, Feline / physiology*
  • Membrane Proteins / chemistry
  • Membrane Proteins / genetics
  • Membrane Proteins / physiology*
  • Molecular Sequence Data
  • Muridae
  • Protein Sorting Signals / chemistry
  • Protein Sorting Signals / genetics
  • Protein Sorting Signals / physiology
  • Receptors, Virus / chemistry
  • Receptors, Virus / genetics
  • Receptors, Virus / physiology*
  • T-Lymphocytes / metabolism
  • T-Lymphocytes / virology
  • Tumor Cells, Cultured


  • FeLIX protein, feline leukemia virus
  • Membrane Proteins
  • Protein Sorting Signals
  • Receptors, Virus
  • leukemia virus receptor, gibbon ape

Associated data

  • GENBANK/AF226623