In most cases, infection starts in the oropharynx where FeLV infects individual lymphocytes that are transported to the bone marrow. Once the rapidly dividing bone marrow cells become infected, large amounts of virions are produced and as a consequence viraemia develops within a few weeks of infection. Often, viraemia may develop several months after constant exposure to shedding cats [Lutz et al., 1983b]. Viraemia leads to the infection of salivary glands and intestinal linings, and virus is shed in large quantities in saliva and faeces [Rojko et al., 1979].
Frequently, the development of viraemia as well as established viraemia may be overcome by a functioning immune system (transient viraemia) [Lutz et al., 1980a]. Such cats (so-called “regressor” cats) are generally not at risk of developing disease. In a multicat household without control of FeLV infection, 30-40 % of the cats develop persistent viraemia, 30-40 % exhibit transient viraemia and 20-30 % seroconvert without ever being detectably viraemic. A smaller proportion (~5 %) exhibits an atypical course of infection showing antigenaemia but no viraemia [Hoover et al 1977]. A cat that has overcome viraemia remains latently infected, i.e. from some cells that remain provirus-positive infectious virus can be recovered when for instance bone marrow cells are kept in cell culture for several weeks [Rojko et al., 1982]. Reactivation may also take place in vivo when latently infected cats experience immune suppression or chronic severe stress [Boretti et al., 2004]. It is not clear how often this happens but it is generally believed to be a rare occurrence.
Generally, up to 10 % of all feline blood samples submitted to a laboratory prove to be provirus-positive and p27 negative, and as in some of these cats, FeLV may be reactivated, they should be considered latently infected [Boretti et al., 2004]. It appears likely that no cat can completely clear FeLV infection from all cells. This might explain why virus neutralising antibodies persist in recovered cats for many years in the absence of overt infection, or exposure to viraemic cats. If this is the case, the risk of such latent persistence leading to reexcretion of virus or the development of disease, must be extremely low since recovered cats appear to have the same life expectancy as cats that have never been exposed to FeLV.
However, proviral DNA has been found in the tumours of ostensibly FeLV-free cats [Jackson et al., 1993], suggesting that the virus might be involved in an early event in the pathogenesis of the tumour and then persist only as a provirus, possibly in a defective form. Local foci of infections or latent virus may also be the source of the FeLV p27 antigen that is sometimes found in the plasma of cats from which infectious virus cannot be isolated, the so-called ‘discordant’ cats.
The typical clinical signs of FeLV infection usually develop in viraemic cats, sometimes not until after several years of viraemia [Hardy et al., 1976].