EVALUATION OF IN-VIVO AND IN-VITRO INTERACTIONS OF FELINE IMMUNODEFICIENCY VIRUS AND FELINE LEUKEMIA-VIRUS

Objective: To determine the potential mechanisms for disease potentiat ion where feline immunodeficiency virus (FIV) infection of persistentl y feline leukemia virus (FeLV)-infected cats results in more severe FI V disease and increased mortality than FIV infection of specific patho gen-free cats. Design and methods: To determine whether pseudotype for mation resulting in expanded cell tropism may be an important mechanis m, cellular targets and tissue distribution of FIV and FeLV were deter mined by in situ hybridization and/or immunohistochemistry. To determi ne whether FeLV can transactivate the FIV long terminal repeat (LTR) r esulting in increased FIV expression, in vitro transient expression as says were performed. To examine whether persistent FeLV infection c,an cause the deletion of a suppressive T-lymphocyte population, peripher al blood mononuclear cell (PBMC) cultures from persistently FeLV-infec ted cats were infected with FIV and monitored for FIV antigen levels. Results: Macrophages were the predominant target of FIV infection and were disseminated in a similar pattern in lymphoid and nonlymphoid tis sues of both FIV-infected and FeLV/FIV-coinfected cats. FeLV-infected cells expressing FIV RNA were not present. Significant transactivation of the FIV LTR in FeLV-infected cells was not demonstrated. FIV antig en production was similar upon in vitro infection of PBMC from FeLV-in fected and uninfected cats. Conclusions: Neither direct virus/virus in teractions, such as FeLV/FIV pseudotype formation or transactivation o f the FIV LTR in FeLV-infected cells, nor deletion of a regulatory cel l subset from the blood of FeLV-infected cats, was found to be the mec hanism of disease potentiation.