PATHOGENESIS OF EXPERIMENTAL FELINE LEUKEMIA-VIRUS INFECTION

Early events In the pathogenesis of feline leukemia virus (FeLV) Infection were studied In 59 specific-pathogen-free cats. Young cats (≤8 wk old and highly susceptible to FeLV) and adult cats (>6 mo old and relatively resistant to FeLV) were exposed to FeLV by oral-nasal, Ip, or sc inoculation. The sequential distribution of FeLV group-specific antigen (GSA) in blood and tissues of susceptible versus resistant cats was correlated with alterations in hematologic and serologic parameters. Six sequential phases of FeLV Infection (I.e., viral replication) were identified: 1) lymphoretlcular cells In local lymphoid tissues [2–14 days after exposure (DAE)]; 2) circulating lymphocytes and monocytes (early cell-associated viremla) (1-14 DAE); 3) lymphoid germinal cells in lymphoid tissues throughout the body (3–12 DAE); 4) bone marrow neutrophil and platelet precursor cells and intestinal crypt epithelium (7–21 DAE); 5) circulating neutrophils and platelets (with establishment of vlremia) (≥14–28 DAE); and 6) mucosal and glandular epithelial tissues (with excretion of FeLV) (≥28–56 DAE). Early lymphoretlcular virus replication (phases 1–3) was present in both progressive and transient Infection. In cats that became persistently infected (80% of young cats and 14% of adult cats), FeLV infection was not contained In the initial lymphoretlcular phases 1-3, and extensive virus replication occurred in the germinal cell populations of lymphoid, hematopoietic, and epithelial tissues (phases 3–6). In cats with progressive Infections, lymphopenia and neutropenia (21–56 DAE) were associated with the appearance of FeLV GSA in circulating neutrophils and platelets (≥14–28 DAE). In cats with self-limiting infections, virus containment in phases 3 or 4 correlated with transient lymphopenia (7–14 DAE) and development of antibody to the feline oncornavirus-associated cell membrane antigen. © 1979, Oxford University Press.