Evaluation of in vivo and in vitro interactions of feline immunodeficiency virus and feline leukemia virus

Amy M. Beebe, Tobie G. Faith, E. Elizabeth Sparger, Michael Torten, Niels C Pedersen, Satya Dandekar

Research output: Contribution to journalArticle

13 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)873-878
Number of pages6
JournalAIDS
Volume8
Issue number7
StatePublished - Jul 1994

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Feline Leukemia Virus
Feline Immunodeficiency Virus
Virus Diseases
Cats
Terminal Repeat Sequences
Blood Cells
In Vitro Techniques
Transcriptional Activation
Viruses
Specific Pathogen-Free Organisms
Antigens
Tropism

Keywords

  • Cellular targets
  • Cofactors
  • Feline immunodeficiency virus
  • Feline leukemia virus
  • Immunohistochemistry
  • In situ hybridization
  • Pseudotypes
  • Transactivation

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Evaluation of in vivo and in vitro interactions of feline immunodeficiency virus and feline leukemia virus. / Beebe, Amy M.; Faith, Tobie G.; Sparger, E. Elizabeth; Torten, Michael; Pedersen, Niels C; Dandekar, Satya.

In: AIDS, Vol. 8, No. 7, 07.1994, p. 873-878.

Research output: Contribution to journalArticle

Beebe, Amy M. ; Faith, Tobie G. ; Sparger, E. Elizabeth ; Torten, Michael ; Pedersen, Niels C ; Dandekar, Satya. / Evaluation of in vivo and in vitro interactions of feline immunodeficiency virus and feline leukemia virus. In: AIDS. 1994 ; Vol. 8, No. 7. pp. 873-878.
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AU - Faith, Tobie G.

AU - Sparger, E. Elizabeth

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AU - Pedersen, Niels C

AU - Dandekar, Satya

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N2 - 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.

AB - 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.

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KW - Immunohistochemistry

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