Abstract

Feline leukemia virus (FeLV) belongs to the genus Gammaretrovirus of the family Retroviridae. FeLV remains a significant pathogen of the domestic cat although its prevalence has been reduced in some populations by removal of infected animals and the development of effective vaccines. Resistance to FeLV is age-related, with later exposure more likely to lead to control of infection via cellular and humoral immunity. This pattern contrasts with feline immunodeficiency virus where infection rates rise directly with age and infection is not cleared. Animals that become persistently viremic with FeLV are at high risk of succumbing to immunosuppressive or neoplastic diseases, particularly of hematopoietic origin. FeLV isolates can be classified in vitro according to envelope type and host receptor specificity, with alternative host range variants (B, C, D and T) arising from the parental subgroup A FeLV by mutation of receptor-binding domains or by recombination with endogenous FeLV or ERV-DC-related sequences in the cat germline. Evolution of these variants is important in the pathogenesis of FeLV as they may lead to acute disease onset. FeLV oncogenesis involves insertional mutagenesis and recombination between FeLV and host proto-oncogenes leading to the formation of feline sarcoma viruses or lymphoma-inducing variants.

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