Publikationsdatum:
2004-02-21
Beschreibung:
Feline immunodeficiency virus (FIV) induces a disease similar to acquired immunodeficiency syndrome (AIDS) in cats, yet in contrast to human immunodeficiency virus (HIV), CD4 is not the viral receptor. We identified a primary receptor for FIV as CD134 (OX40), a T cell activation antigen and costimulatory molecule. CD134 expression promotes viral binding and renders cells permissive for viral entry, productive infection, and syncytium formation. Infection is CXCR4-dependent, analogous to infection with X4 strains of HIV. Thus, despite the evolutionary divergence of the feline and human lentiviruses, both viruses use receptors that target the virus to a subset of cells that are pivotal to the acquired immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimojima, Masayuki -- Miyazawa, Takayuki -- Ikeda, Yasuhiro -- McMonagle, Elizabeth L -- Haining, Hayley -- Akashi, Hiroomi -- Takeuchi, Yasuhiro -- Hosie, Margaret J -- Willett, Brian J -- R01 AI49765-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 20;303(5661):1192-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterinary Microbiology, Graduate School of Agricultural and Life Sciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976315" target="_blank"〉PubMed〈/a〉
Schlagwort(e):
Amino Acid Sequence
;
Animals
;
CD4-Positive T-Lymphocytes/immunology/metabolism/virology
;
Cats
;
Cell Line
;
Cell Line, Tumor
;
DNA, Complementary
;
Gene Library
;
HIV/metabolism
;
HeLa Cells
;
Heterocyclic Compounds/pharmacology
;
Humans
;
Immunodeficiency Virus, Feline/*metabolism/pathogenicity
;
Mice
;
Molecular Sequence Data
;
NIH 3T3 Cells
;
Receptors, CXCR4/antagonists & inhibitors/metabolism
;
Receptors, OX40
;
Receptors, Tumor Necrosis Factor/chemistry/genetics/immunology/*metabolism
;
Receptors, Virus/chemistry/genetics/immunology/*metabolism
;
Species Specificity
;
Transduction, Genetic
;
Transfection
Print ISSN:
0036-8075
Digitale ISSN:
1095-9203
Thema:
Biologie
,
Chemie und Pharmazie
,
Informatik
,
Medizin
,
Allgemeine Naturwissenschaft
,
Physik
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