Search

The purpose of this study was to determine the tissue distribution and antiviral activity of the CD8 lymphocytes that suppress the replication of feline immunodeficiency virus (FIV). Cell-associated FIV load, CD8alpha(+)beta(low) cells, and CD8 cell-mediated suppression of FIV were measured serially in the blood, thymus, and peripheral lymph nodes after neonatal inoculation. Between 6 and 10 weeks, relative numbers of CD8alpha(+)beta(low) cells increased, whereas CD8alpha(+)beta(high) cells declined in the thymus and blood of infected cats. By 12-16 weeks, the lymph nodes were enlarged because of an absolute expansion of all CD8beta subpopulations. The strength of CD8 cell-mediated FIV suppression in vitro, but not CD8alpha(+)beta(low) cell content, was correlated inversely with virus load in the thymus and blood. Thus, after neonatal FIV inoculation, CD8alpha(+)beta(low) cells first occupy the thymus and blood, where strong CD8 cell-mediated antiviral activity is linked to reduced virus load in multiple lymphoid tissues.

Similar to human immunodeficiency virus type 1, feline immunodeficiency virus (FIV) replicates in the thymus of infected animals, causing marked alteration in thymic lymphocyte subpopulations. The immune phenotype and cytokine patterns in the thymus and secondary lymphoid tissues of FIV-infected cats were investigated. FIV infection caused an acute-stage transient reduction in CD4CD8 double-positive thymocytes, a marked increase in CD8 single-positive thymocytes, and formation of thymic B cell lymphoid follicles. Interferon (IFN)-gamma and interleukin (IL)-10 mRNA were up-regulated in both the thymus and lymph nodes of FIV-infected cats. Analysis of purified CD4 and CD8 cells revealed that CD4 cells produced most of the IL-10, whereas IFN-gamma was produced by both subsets. Quantitative-competitive reverse-transcription polymerase chain reaction analysis revealed that thymocytes, especially CD4CD8 thymocytes, had much greater levels of gag mRNA than did lymph node T cells. Thus, overexpression of IFN-gamma and IL-10 is a feature of the thymus and secondary lymphoid tissues of FIV-infected cats.

Similar to human immunodeficiency virus, feline immunodeficiency virus (FIV) induces immunodeficiency and enhanced susceptibility to secondary pathogens. To explore cytokine alterations in lentivirus immunodeficiency, constitutive mRNA expression was measured in lymph nodes of healthy and FIV-infected cats before and after challenge with Toxoplasma gondii. Cytokine mRNA expression was similar in control and FIV-infected cats during the first 10 weeks after infection. At 16 weeks, interferon (IFN)-gamma, tumor necrosis factor-alpha, and interleukin (IL)-10 mRNA were increased in FIV-infected cats. Challenge with T. gondii induced an increase in IL-2, IFN-gamma, and IL-12 in the lymph nodes of control cats, whereas IFN-gamma and IL-10 but not IL-2 or IL-12 increased in the lymph nodes of FIV-T. gondii coinfected cats. These results indicate that FIV immunodeficiency may derive from a failure to generate an IL-12-dependent type 1 response and that an elevated level of IL-10 mRNA expression is a predictor of lentivirus immunodeficiency.

Netilmicin was found to be less toxic than gentamicin when administered at comparable dosage levels to squirrel monkeys (Saimiri sciureus). This finding is based upon data obtained from the following determinations: length of survival period; change in body weight; observation of general change in behavior after daily injection; ataxia, as measured by the squirrel monkey platform-runway test; acoustic reflex threshold; levels of blood urea nitrogen and serum creatinine (and pathology of the kidney); and microbiological antibiotic assay.