Feline leukemia/sarcoma viruses and immunodeficiency

Abstract

This chapter discusses the structure feline leukemia virus (FeLV) and pathogenesis of lymphomas and leukemias BY FeLV. FeLV is quite similar to the better-studied murine leukemia viruses in structure and genetic map. The virus particles bud from cytoplasmic membranes into either extracellular spaces or into vacuoles. FeLV has long been considered a typical noncytopathogenic, longlatency leukemia virus based on its behavior in fibroblasts in vitro. Recent evidence suggests that its in vivo behavior in critical target hemolymphatic tissues is as likely to be cytopathic as transforming. The type of FeLV-related disease that occurs and the disease-free interval probably are influenced by viral envelope proteins and glycoproteins and the consequences of proviral integration. FeLV subgroup specificity apparently determines when and what type of disease will occur. The ecotropic FeLV-A is the most frequent subgroup found in pet cats and is transmitted contagiously. Immunosuppression is the most frequent and the most devastating manifestation of FeLV viremia in clinical and experimental studies. It seems that multiple cell types and multiple processes are involved in the development of feline retrovirus-induced immunosuppression. Although no solid evidence is available for the malfunctioning of cat T helper cells because of the paucity of T-cell specific markers, the circumstantial evidence provided thus far indicates an impaired T helper function in FeLV-infected cats similar to that observed in humans infected with HIV. Studies on the pathogenesis of FeLV-induced immunosuppression might provide a valuable mode for a better understanding and means of control of human AIDS.