The molecular biology of feline immunodeficiency virus (FIV)

Abstract

Feline immunodeficiency virus (FIV) is widespread in feline populations and causes an AIDS-like illness in domestic cats. It is highly prevalent in several endangered feline species. In domestic cats FIV infection is a valuable small animal model for HIV infection. In recent years there has been sa significant increase in interest in FIV, in part to exploit this, but also because of the potential it has as a human gene therapy vector. Though much less studied than HIV there are many parallels in the replication of the two viruses, but also important differences and, despite their likely common origin, the viruses have in some cases used alternative strategies to overcome similar problems. Recent advances in understanding the structure and function of FIV RNA and proteins and their interactions has enhanced our knowledge of FIV replication significantly, however, there are still many gaps. This review summarizes our current knowledge of FIV molecular biology and its similarities with, and differences from, other lentiviruses.

Keywords: FIV; retrovirus, lentivirus.

Figure 1.

The organisation of the FIV genome. Genes and LTRs are shown roughly to scale. pol is translated from the full length RNA as a fusion Gag/Pol protein through a frameshift. LTR long terminal repeat; MA, matrix; CA, capsid; NC, nucleocapsid; PR, protease; RT, reverse transcriptase; DU, dUTPase; IN, integrase. cis acting RNA elements are shown above: ψ, packaging signal (RNA structure shown); mSD, major splice donor; DIS, dimerization initiation site; PBS, primer binding site; RRE, Rev response element. Regulatory elements are shown below in a magnified LTR.

Figure 2.

The feline immunodeficiency virus (FIV) replication cycle. Figure courtesy of Claire Williams.