The virus-receptor interaction in the replication of feline immunodeficiency virus (FIV)

- Expression of viral receptor CD134 is consistent with FIV cell tropism.
- Differential usage of CD134 by individual strains of FIV defined by requirement for CRD2 of CD134.
- CRD2-dependent strains dominate in early infection.
- CRD2-independent strains emerge in late infection.
- Selective expansion of CRD2-dependent variants following experimental transmission.

The feline and human immunodeficiency viruses (FIV and HIV) target helper T cells selectively, and in doing so they induce a profound immune dysfunction. The primary determinant of HIV cell tropism is the expression pattern of the primary viral receptor CD4 and co-receptor(s), such as CXCR4 and CCR5. FIV employs a distinct strategy to target helper T cells; a high affinity interaction with CD134 (OX40) is followed by binding of the virus to its sole co-receptor, CXCR4. Recent studies have demonstrated that the way in which FIV interacts with its primary receptor, CD134, alters as infection progresses, changing the cell tropism of the virus. This review examines the contribution of the virus-receptor interaction to replication in vivo as well as the significance of these findings to the development of vaccines and therapeutics.