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SUMMARYThe chemiluminescent characteristics of enriched (>95%) peripheral blood polymorphonuclear leukocyte populations (PMN) from normal and feline leukaemia virus (FeLV)-infected cats were investigated. FeLV-infected cats demonstrated a significantly lower (P < 0.001) PMN chemiluminescent response when compared to the response of normal age-matched controls. Normal PMN treated with FeLVinfected cat serum exhibited a depressed response in comparison to control cells. A titration of serum from infected cats supplemented with normal serum revealed a titratable suppression of chemiluminescence with increasing concentration of serum from the infected cats. However, PMN from FeLV-infected cats treated with normal serum displayed a slight increase in chemiluminescence over the same cells in autologous serum. The addition of inactivated FeLV to normal PMN caused a titratable decrease in chemiluminescence.

Polymorphonuclear leukocytes (PMN) from healthy, normal control cats and FeLV-infected cats were analyzed for differences in phagocytic capabilities. One week after experimental infection, PMNs from FeLV-infected cats exhibited a marked decrease in phagocytic function as determined by the luminol-dependent chemiluminescent response. Depressed PMN function was observed in these cats during the viremic stage of infection and subsequently remained depressed after the cessation of viremia. The data presented here suggest that while nonviremic cats are reported as clinically normal, they may in fact be exhibiting a suppressed PMN function.

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Experimental infection with the Mt. Airy isolate of feline immunodeficiency virus (FIVMA), a lentivirus isolated from a domestic cat exhibiting signs of an immunodeficiency-like syndrome, results in transient lymphadenopathy, fever, stomatitis, enteritis, neurologic abnormalities, and immunosuppression. The effects of FIVMA infection on neutrophil and natural killer cell (NK) function were examined in vitro. Suppression of neutrophil chemiluminescence (CL) responses, as well as reduction in NK-mediated cytotoxicity were demonstrated. Neutrophil CL was decreased by 50% in infected cats when compared to control values. This loss of CL was present through 6 months after infection. In addition, NK-mediated cytotoxicity was approximately 50% less in FIVMA infected cats than in controls. Loss of innate immunity was paralleled with inversion in feline CD4/CD8 lymphocyte ratios and decreases in lymphocyte mitogenesis seen as early as 5 weeks after infection. These results suggest that FIVMA infection induces an immunodeficiency disorder in infected cats similar to that seen in human immunodeficiency virus infections.

This is a review of the current knowledge of feline leukemia virus (FeLV) associated with immune depression observed in cats. It will focus on the clinical and experimental observations associated with feline retroviral infection and presence in vivo and in vitro. We will briefly describe retroviral-associated acquired immune deficiency syndrome associated with FeLV infection in the cat and specific cellular pathology associated with FeLV latency. In addition, we will focus on the action of FeLV-p15E in vitro and describe possible mechanisms of the FeLV-associated immunosuppression observed both in vivo and in vitro. Lastly, we will evaluate the current status of immunoprevention of FeLV. We will not attempt an in-depth analysis of the current literature; our focus is to review current findings as they relate to feline AIDS and immunotherapy.

Receptor-mediated activation is accompanied by phospholipid metabolism and by calcium fluctuation resulting in a chemiluminescence (CL) response in the neutrophil. This pathway involves activation of protein kinase C (PKC) and the NADPH oxidase. Artificial stimulants such as phorbol esters, specifically 12-O-tetradecanylphorbol-13-acetate (TPA), circumvent the receptor-mediated pathway and activate PKC resulting in a measurable CL response. Neutrophils from feline leukemia virus (FeLV) exposed cats were tested for their ability to generate a TPA-induced CL response. As compared to the non-FeLV-exposed specific-pathogen-free (SPF) control cat neutrophil CL responses, both viremic and nonviremic FeLV-exposed cats showed significant decreases in their CL responsiveness. Neither ultraviolet light-inactivated FeLV (UV-FeLV) nor protein components (FeLV-p15E and FeLV-p27) caused a significant decrease in the CL responses of the SPF cat neutrophils. The suppressed TPA-induced CL response from FeLV-infected cats may involve an intracellular mechanism not affected in vitro by exposure of the neutrophil to the virus or viral components.

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