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Accessing Early Differentiation of Virus-Specific Follicular Helper CD4+ T Cell in Acute LCMV-Infected Mice
Published on: April 26, 2024
[Feline immunodeficiency virus tropism]
1Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokendai, Minato-ku, Tokyo 108-8639, Japan. shimoji-@ims.u-tokyo.ac.jp
Insights
Feline immunodeficiency virus (FIV) uses CD134 (OX40) as its primary receptor, unlike HIV which uses CD4. This discovery also aided in identifying entry factors for Ebola virus.
Area of Science:
- Virology
- Immunology
Context:
- 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:
- To identify the primary cellular receptor for Feline Immunodeficiency Virus (FIV).
- To investigate the mechanism of FIV entry and infection.
- To adapt the receptor identification method for other viruses, such as Ebola virus.
Summary:
- Feline immunodeficiency virus (FIV) primarily uses CD134 (OX40), a T cell activation molecule, for viral binding, entry, and infection.
- FIV infection is dependent on CXCR4, similar to X4-tropic HIV strains.
- The study identified Axl and Dtk (Tyro3 family) as Ebola virus entry factors using a modified method.
Impact:
- Elucidates the molecular mechanisms of FIV pathogenesis.
- Reveals convergent evolution in lentiviral receptor usage.
- Provides a novel method for identifying viral entry factors, applicable to emerging infectious diseases like Ebola virus.
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. Further, we applied the new method for FIV receptor to Ebola virus entry factors with some modifications, and identified receptor-type tyrosine kinases, Axl and Dtk (members of Tyro3 family). Distribution of the molecules matches well with the Ebola virus tropism.
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