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Blood, Vol. 95 No. 3 (February 1), 2000:
pp. 1093-1099
Cloning of the cellular receptor for feline leukemia virus
subgroup C (FeLV-C), a retrovirus that induces red cell aplasia
John G. Quigley,
Cara C. Burns,
Maria M. Anderson,
Eric D. Lynch,
Kathleen M. Sabo,
Julie Overbaugh, and
Janis L. Abkowitz
From the Divisions of Hematology, Microbiology, and Medical
Genetics, Department of Medicine, University of Washington, Seattle;
and Division of Human Biology, Fred Hutchinson Cancer Research Center,
Seattle, WA.
Feline leukemia virus-C (FeLV-C) causes red cell aplasia in cats,
likely through its interaction with its cell surface receptor. We
identified this receptor by the functional screening of a library of
complementary DNAs (cDNA) from feline T cells. The library, which was
cloned into a retroviral vector, was introduced into FeLV-C-resistant
murine (NIH 3T3) cells. The gene conferring susceptibility to FeLV-C
was isolated and reintroduced into the same cell type, as well as into
FeLV-C-resistant rat (NRK 52E) cells, to verify its role in viral
infection. The receptor cDNA is predicted to encode a protein of 560 amino acids with 12 membrane-spanning domains, termed FLVCR. FLVCR has
significant amino acid sequence homology with members of the major
facilitator superfamily and especially D-glucarate transporters
described in bacteria and in C. elegans. As FeLV-C impairs the
in vivo differentiation of burst-forming unit-erythroid to
colony-forming unit-erythroid, we hypothesize that this transporter
system could have an essential role in early erythropoiesis. In further
studies, a 6-kb fragment of the human FLVCR gene was amplified by
polymerase chain reaction from genomic DNA, using
homologous cDNA sequences identified in the human Expressed Sequence
Tags database. By radiation hybrid mapping, the human gene was
localized to a 0.5-centiMorgan region on the long arm of chromosome 1 at q31.3.
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