Lymph Node Pathology in Experimental Fiv Infection

Abstract

Feline immunodeficiency virus (FIV) was first isolated in 1986 from a colony of cats in California exhibiting multiple, and often chronic, infections (Pedersen et al, 1987). The virus was characterised as a T-lymphotropic lentivirus morphologically similar but antigenically distinct from human immunodeficiency virus (HIV), the cause of acquired immunodeficiency syndrome (AIDS) in man (Barré-Sinoussi et al, 1983; Gallo et al, 1984). Subsequently the virus was isolated throughout the world (Harbour et al, 1988; Ishida et al, 1988) and analysis of stored serum samples indicated that FIV infection has been present since at least the 1960s in cat populations (Gruffydd-Jones et al, 1988; Shelton et al, 1990). It is likely that biting is the most common means of transmission of the virus (Yamamoto et al, 1989). Infection is persistent and can be detected by the demonstration of infectious virus in activated T cells from peripheral blood (Pedersen et al, 1987), by amplification of FIV nucleic acid sequences in blood or other cells by the polymerase chain reaction (PCR) (Dandekar et al, 1992) or by the demonstration of anti-FIV antibodies in the serum or plasma (Pedersen et al, 1987; Hosie & Jarrett, 1990).