Feline leukaemia virus (FeLV) is a gamma retrovirus affecting domestic cats worldwide; it was first detected in 1964 by electron microscopy after experimental transmission by cell-free material [Jarrett et al. 1964]. FeLV also infects small wild cats including Felis silvestris and European and Iberian lynxes.
All retroviruses, including FeLV, are enveloped RNA viruses and rely on a DNA intermediate for replication. The single-stranded RNA genome is reverse transcribed into DNA, which is usually integrated into the host's cell genome with an integrase [Temin & Mizutani 1970]. The integrated DNA is known as provirus. After reverse transcription, synthesis of viral proteins occurs according the conventional mechanisms of transcription with assembly of the virions near the cell membrane and budding from the cell [Coffin 1979]. Infection of a cell by a retrovirus does not usually lead to cell death.
The FeLV genome contains three genes: envelope (env) coding for the glycoprotein gp70 (SU) and the transmembrane protein p15 (E) (TM), the polymerase (pol) gene coding for reverse transcriptase, protease and integrase, and the group specific antigen (gag) gene coding for the structural proteins of the virus including p27 [Coffin 1979]. Besides this so-called exogenous FeLV, in the domestic cat two forms of endogenous gamma retroviruses are known: the endogenous feline leukaemia virus (enFeLV) [Soe et al., 1983] and the RD114 virus [Sarma et al., 1973].
The enFeLV is thought to have originated hundred thousands of years ago from cats that had eaten mice viraemic with a murine leukaemia virus (MuLV) which was able to incorporate its genome into the germ line cells of the predator. This MuLV was then inherited by all the offspring. The amount of enFeLV varies between different breeds of cats including Felis silvestris suggesting that this exposure to MuLVs is a continuing phenomenon [Tandon et al., 2007]. The enFeLV genome is not complete and therefore it is not competent to replicate by its own [Soe et al., 1983].
The RD114 virus is of primate origin, replication competent, and thought to have originated hundred thousands of years ago from an ancestor cat that had preyed on an early primate infected with this RD114 virus [Barbacid et al., 1977]. Feline cells are not susceptible to RD114 virus, and this virus has no pathogenic potential for cats.
FeLV exists in four subtypes: A, B, C, and T [Anderson et al., 2000; Russell & Jarrett 1978]. The subtypes are defined by host cell spectrum; they are immunologically closely related. The subtype A is ubiquitous and is involved in every infection. Subtype B originates from recombination of FeLV A with enFeLV. Subtype C is the result of mutations in the env gene, and subtype T has a tropism for T lymphocytes.
FeLV does not survive for long outside the host as it is destroyed readily by disinfectants, soap, heating and drying. Transmission via fomites is unlikely. The virus will survive, however, if it is kept moist at room temperature so that there is potential for iatrogenic transmission to occur via contaminated needles, surgical instruments or blood transfusions.
FeLV occurs worldwide. Its prevalence may be influenced by the density of cats and there
may be noticeable geographical and local variation. There is little reliable information on the
current prevalence of FeLV in different countries. In some European countries, the USA and
Canada, the prevalence of FeLV infection in individually kept cats seems to be very low,
usually less than 1 % [Hosie et al., 1989; Levy et al., 2006; Lutz et al., 1990]. In large multicat
households without specific preventive measures for introduction of FeLV, the prevalence
may be greater than 20 %.
Over the last 25 years, the prevalence and importance of FeLV infection in Europe has greatly
diminished due to the availability of reliable tests, the test and removal programmes initiated,
improved understanding of the pathogenesis and the introduction of highly efficacious FeLV
vaccines.
Cats with FeLV viraemia act as a source of infection. Virus is shed from an infected cat in
saliva, nasal secretions, faeces, and milk [Hardy et al., 1976; Pacitti et al., 1986]. Risk factors
for infection are young age, high population density and poor hygiene. FeLV infection is
transmitted mainly by mutual grooming, but also through bites. In viraemic queens,
pregnancy usually results in embryonic death, stillbirth or in viraemic kittens which fade
away rapidly. In latently infected queens, usually transmission does not take place during
pregnancy. However rarely, some (but not all) kittens may become viraemic after birth
[Pacitti et al., 1986]. In these instances, transmission takes place from individual mammary
glands where the virus can remain latent until the mammary gland develops during the last
period of pregnancy. Young kittens are especially susceptible to FeLV infection while with
age, cats become increasingly resistant to infection [Hoover et al., 1976; Grant et al. 1980].
Although aged cats are generally accepted to be more resistant to infection, they can still be
infected providing the challenge is sufficiently severe.