Abstract
Feline leukemia virus (FeLV) infection is transmissible by contact exposure, by oral-nasal or parenteral inoculation, and by congenital exposure of outbred cats to FeLV. The susceptibility vs resistance of cats to FeLV is determined by early containment vs amplification of retroviral replication in target hemolymphatic cells. The course of these pivotal early events is age-dependent, macrophage-dependent, and corticosteroid-sensitive. Either of two host-virus relationships ensue in cats exposed to FeLV: (a) progressive infection characterized by persistent viral replication in hemolymphatic and epithelial cells, persistent viremia, minimal anti-viral immune response, and a high risk of subsequent disease, or (b) regressive infection characterized by transient retroviral replication in hemolymphatic cells, abrogation of viremia, and a low incidence of subsequent disease. Some regressively infected cats harbor persistent latent FeLV infection in certain hemolymphatic cells. Such residual non-productive FeLV infections may be reactivated, transmitted congenitally, or be involved in the genesis of virus-negative leukemias. Although less notorious than leukemogenesis, it is the cytosuppressive disease syndromes which constitute the predominant pathogenic manifestations of FeLV infection in cats.
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