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Published on: March 12, 2015
Use of CD134 as a primary receptor by the feline immunodeficiency virus
Masayuki Shimojima1, Takayuki Miyazawa, Yasuhiro Ikeda
1Department of Veterinary Microbiology, Graduate School of Agricultural and Life Sciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan.
Insights
Feline immunodeficiency virus (FIV) uses CD134 (OX40) as its primary receptor, unlike HIV which uses CD4. This discovery sheds light on FIV
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Feline immunodeficiency virus (FIV) causes an AIDS-like illness in cats.
- Unlike human immunodeficiency virus (HIV), FIV does not utilize CD4 as its primary receptor.
Purpose of the Study:
- To identify the primary cellular receptor for Feline Immunodeficiency Virus (FIV).
- To understand the mechanism of FIV entry and infection.
Main Methods:
- Identification of FIV viral receptor through cellular expression analysis.
- Assessment of CD134's role in viral binding, entry, and infection.
Main Results:
- CD134 (OX40), a T cell activation antigen, was identified as the primary receptor for FIV.
- CD134 expression facilitates FIV binding, entry, infection, and syncytium formation.
- FIV infection is dependent on CXCR4, similar to X4-tropic HIV strains.
Conclusions:
- FIV utilizes CD134 as its primary receptor, distinct from HIV's CD4 receptor.
- Both feline and human lentiviruses target critical immune cells via specific receptor interactions.
- This finding deepens the understanding of lentiviral entry mechanisms and host-specific tropism.
Abstract:
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.
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