Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
Evaluation of in vivo and in vitro interactions of feline immunodeficiency virus and feline leukemia virus.
AIDS. 1994 Jul;8(7):873-8. Unique Identifier : AIDSLINE MED/95032916 Beebe AM; Faith TG; Sparger EE; Torten M; Pedersen NC; Dandekar S; Department of Internal Medicine, School of Medicine, University; of California, Davis 95616.
Abstract:
OBJECTIVE: To determine the potential mechanisms for disease potentiation where feline immunodeficiency virus (FIV) infection of persistently feline leukemia virus (FeLV)-infected cats results in more severe FIV disease and increased mortality than FIV infection of specific pathogen-free cats. DESIGN AND METHODS: To determine whether pseudotype formation resulting in expanded cell tropism may be an important mechanism, cellular targets and tissue distribution of FIV and FeLV were determined by in situ hybridization and/or immunohistochemistry. To determine whether FeLV can transactivate the FIV long terminal repeat (LTR) resulting in increased FIV expression, in vitro transient expression assays were performed. To examine whether persistent FeLV infection can cause the deletion of a suppressive T-lymphocyte population, peripheral blood mononuclear cell (PBMC) cultures from persistently FeLV-infected 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 tissues 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 antigen production was similar upon in vitro infection of PBMC from FeLV-infected and uninfected cats. CONCLUSIONS: Neither direct virus/virus interactions, such as FeLV/FIV pseudotype formation or transactivation of the FIV LTR in FeLV-infected cells, nor deletion of a regulatory cell subset from the blood of FeLV-infected cats, was found to be the mechanism of disease potentiation.
Keywords: Animal Cats Cells, Cultured Feline Acquired Immunodeficiency Syndrome/*COMPLICATIONS/ MICROBIOLOGY Gene Expression Regulation, Viral Immunodeficiency Virus, Feline/GENETICS/*PHYSIOLOGY In Situ Hybridization Leukemia Virus, Feline/GENETICS/*PHYSIOLOGY Leukemia, Feline/*COMPLICATIONS/MICROBIOLOGY Macrophages/MICROBIOLOGY Repetitive Sequences, Nucleic Acid RNA, Viral/ANALYSIS Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. T-Lymphocytes/MICROBIOLOGY Trans-Activation (Genetics) Viral Interference JOURNAL ARTICLE 950228
M9521010
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