When community-source cats, cats allowed outdoors, or cats exposed to fleas are to be used as blood donors, they should be regularly assessed for infection with M haemofelis, 'Candidatus M haemominutum,' and Bartonella spp, and flea-control treatment should be regularly provided.

No abstract

This study was designed to test the effect of antioxidant supplementation on feline immunodeficiency virus (FIV)-infected felines. Six acutely FIV-infected cats (> or =16 weeks post-inoculation) were given a propriety oral superoxide dismutase (SOD) supplement (Oxstrin; Nutramax Laboratories) for 30 days. Following supplementation, the erythrocyte SOD enzyme concentration was significantly greater in the supplemented FIV-infected group than the uninfected control group or the unsupplemented FIV-infected group. The CD4+ to CD8+ ratio increased significantly (0.66-0.88) in the SOD supplemented FIV-infected cats but not in the unsupplemented FIV-infected cats. Proviral load and reduced glutathione (GSH) levels in leukocyte cell types did not change significantly following supplementation. Antioxidant supplementation resulted in an increase in SOD levels, confirming the oral bioavailability of the compound in FIV-infected cats. This result warrants further investigation with trials of antioxidant therapy in FIV-infected cats that are showing clinical manifestations of their disease, as well as in other feline patients where oxidative stress likely contributes to disease pathogenesis, such as diabetes mellitus and chronic renal failure.

Summary Impaired dendritic cell (DC) function is thought to be central to human immunodeficiency virus‐associated immunodeficiency. In this study, we examined the effect of chronic feline immunodeficiency virus (FIV) infection on DC cytokine production in response to microbial and T‐cell stimulation. Cytokine production after either Toll‐like receptor (TLR) or CD40 ligation in bone marrow‐derived DCs (BM‐DCs) was measured in naïve and chronically FIV‐infected cats. The BM‐DCs were stimulated with ligands to TLR‐2, ‐3, ‐4, ‐7 and ‐9 or cocultured with 3T3 cells expressing feline CD40 ligand. Ligation of TLR‐4 and TLR‐9 in BM‐DCs from infected cats resulted in a significant decrease in the ratio of interleukin‐12 (IL‐12) to IL‐10. Conversely, TLR‐7 ligation produced a significant increase in the IL‐12 : IL‐10 ratio in BM‐DCs from infected cats. No difference was noted for TLR‐3 ligation. RNA expression levels of TLR‐2, ‐3, ‐4, ‐7 and ‐9 were not significantly altered by FIV infection. CD40 ligation significantly elevated both IL‐10 and IL‐12 messenger RNA production but did not alter the IL‐12 : IL‐10 ratio. Chronic FIV infection alters the ratio of immunoregulatory cytokines produced by BM‐DCs in response to certain pathogen‐derived signals, which is probably relevant to the increased risk of opportunistic infections seen in lentiviral infection.

Dendritic cells (DC) are potent antigen presenting cells which initiate and coordinate the immune response making them central targets of and attractive candidates for manipulation in chronic lentiviral infections. Emerging evidence suggests that DC immune function is disrupted during both acute and chronic infection with human immunodeficiency virus (HIV), simian immunodeficiency virus (SIV), and feline immunodeficiency virus (FIV). Despite some early promising data, the use of DC for lentiviral immunotherapy has not fulfilled its expected potential and has been complicated by the large number of variables involved in DC harvesting, purifying, and antigen-loading. Pre-clinical studies aimed at identifying successful strategies for DC augmentation of current HIV treatment protocols are needed. Over the past two decades, the FIV model for HIV infection has increased the understanding of retroviral pathogenesis, and studies have begun using the FIV model to study DC dysfunction and DC-mediated immunotherapy. Careful consideration of the many variables involved in DC function and therapy should help develop protocols to explore the potential of DC vaccine-based therapies for lentiviral infection.