Quantification of lymphadenopathy in experimentally induced feline immunodeficiency virus infection in domestic cats.

Nine cats experimentally infected with feline immunodeficiency virus (FIV) and six FIV-negative cats were necropsied to assess the effect of FIV infection on lymph nodes. The FIV infected cats were inoculated with 10(5) TCID50 21-22 weeks previously. The combined weights of all lymph nodes and the combined lymph node to organ weight ratios were significantly greater in FIV-infected cats when compared to uninfected cats. Additionally, by examining all nodes in the body, a regionally severe lymphadenopathy in FIV-infected cats was evident involving the lymph nodes of the hindlimb, forelimb, and head, in decreasing order of severity, with little evidence of enlargement in lymph nodes of the alimentary tract. Use of 99% confidence intervals showed that 9/9 FIV infected cats had enlarged lymph nodes of the hindlimb and forelimb region. In contrast, 7/9 and 3/9 FIV-infected cats exhibited enlargement of the nodes of the head region and alimentary tract, respectively. Similarly the combined weights of both left and right popliteal lymph nodes were enlarged in 9/9 FIV-infected cats whereas 0/6 in uninfected cats were not. The enlargement of the popliteal lymph nodes observed at necropsy was reflected microscopically by an increase in the size and number of germinal centres and an increase in the number of plasma cells, especially in the medullary cords. Because of the regional variation in lymph node size and numbers, it is suggested that the popliteal lymph node is a good indicator node for the assessment of lymph node status in FIV infection.

Evaluation of an autologous red cell agglutination test, VetRED FIV, for the presence of FIV antibody in cats.

A commercially available whole blood agglutination test, VetRED FIV, used for the detection of antibodies to feline immunodeficiency virus (FIV), was evaluated. The test is based on the use of a synthetic peptide conjugated to a non-agglutinating anti-feline red blood cell monoclonal antibody. The amino acid sequence of the synthetic peptide was derived from the predicted sequence of the transmembrane protein of FIV. The sensitivity and specificity of VetRED FIV was 100% when 34 known FIV-positive and 15 known FIV-negative cats were tested. These cats were part of studies on experimentally induced FIV infection, with their FIV status confirmed by virus isolation. Further, VetRED FIV was compared with another commercially available test for FIV antibody, PetChek in a field trial on 548 feline blood samples received by a diagnostic laboratory. Of the test results 94.2% (516/548) were in agreement: 112 were positive by VetRED FIV and PetChek; 404 were negative by both tests and 32 were discordant. These 5.8% discordant samples producing VetRED FIV-positive/PetChek-negative or VetRED FIV-negative/PetChek-positive were further assessed by Western blot assay. In the field trial, the sensitivity and specificity of VetRED FIV was 97% and 97%, respectively, comparable to the 98% sensitivity and 99% specificity for PetChek. The results from the trial also confirm the relatively high overall prevalence of FIV in Australian cats predominantly among mature male cats in the 9-12 year age group. Given the simplicity of the VetRED FIV procedure, it is concluded that VetRED FIV is a useful addition to the available commercial tests for FIV infection.

Feline immunodeficiency virus infection: plasma, but not peripheral blood mononuclear cell virus titer is influenced by zidovudine and cyclosporine.

The plasma and peripheral blood mononuclear cell (PBMC) titer of feline immunodeficiency virus (FIV) in experimentally infected cats was assessed following administration of either zidovudine or cyclosporine. Treatments were begun 24 h post infection (p.i.) and continued for 4 weeks. Zidovudine treatment did not prevent establishment of infection with FIV, but plasma virus titers were significantly lower than controls at 2 weeks p.i. This reduction of plasma virus titer by zidovudine was not maintained at subsequent sampling times. Similarly, cyclosporine treatment initially lowered plasma virus titers at 2 weeks p.i., but at 4 weeks p.i. the plasma virus titers in cyclosporine-treated cats were significantly higher than in the untreated group. In the untreated group, plasma virus titers declined rapidly to an undetectable level by 14 weeks p.i. Neither zidovudine or cyclosporine treatment significantly influenced the titer of FIV in PBMCs. In all groups (untreated, zidovudine and cyclosporine) the titers in PBMC were high for the duration of the experiment. The decline in plasma virus titers in immunocompetent cats combined with the effect of cyclosporine on plasma titers strongly suggest that the immune system plays a major role in clearing FIV from plasma. In contrast, it appears that the immune response has little impact on PBMC virus titers. This shows that for complete assessment of antiviral agents, both cell-free and cell-associated virus titers must be examined. We also suggest that the limitation of viral titers in PBMC may be of critical importance in the control of lentiviral infection.

Feline immunodeficiency virus: quantification in peripheral blood mononuclear cells and isolation from plasma of infected cats.

The titer of feline immunodeficiency virus in peripheral blood mononuclear cells (PBMC) and the presence of infectious virus in plasma was investigated over 20 week period in 8 experimentally infected cats, 3 uninfected cats and 2 naturally infected cats by end point dilution cultures using a feline T-lymphoblastoid cell line (MYA-1). FIV was isolated from PBMC of all infected cats, but not from the uninfected cats. FIV was also isolated consistently from 100 microliters plasma from most of the experimentally infected cats, but not from the 2 naturally infected cats. The virus titer in PBMCs in both experimentally and naturally infected cats was comparatively high, ranging from 10 TCID/10(6) PBMC to 14,286 TCID/10(6) PBMC. The titers in PBMC of individual cats remained unchanged or varied only slightly over the 20 week period. In contrast, the titers varied substantially between cats, with significantly higher titers in the youngest litter (4 cats) than in the oldest litter (3 cats). This suggests that there is an age-related factor influencing the level of PBMC virus titers in experimental infection with FIV. A similar age-related susceptibility has been shown with feline leukemia virus. More importantly, the sustained titers in the experimentally infected cats bear close resemblance to infection of children with human immunodeficiency virus. These data reinforce suggestions that age and immune maturity have a fundamental influence on PBMC and plasma titers in lentivirus infections.