FELINE IMMUNODEFICIENCY VIRUS (FIV)-SPECIFIC CYTOTOXIC T-LYMPHOCYTES FROM CHRONICALLY INFECTED CATS ARE INDUCED IN-VITRO BY RETROVIRAL VECTOR-TRANSDUCED FELINE T-CELLS EXPRESSING THE FIV CAPSID PROTEIN

Citation
Wr. Song et al., FELINE IMMUNODEFICIENCY VIRUS (FIV)-SPECIFIC CYTOTOXIC T-LYMPHOCYTES FROM CHRONICALLY INFECTED CATS ARE INDUCED IN-VITRO BY RETROVIRAL VECTOR-TRANSDUCED FELINE T-CELLS EXPRESSING THE FIV CAPSID PROTEIN, Virology, 209(2), 1995, pp. 390-399
Citations number
57
Categorie Soggetti
Virology
Journal title
ISSN journal
00426822
Volume
209
Issue
2
Year of publication
1995
Pages
390 - 399
Database
ISI
SICI code
0042-6822(1995)209:2<390:FIV(CT>2.0.ZU;2-S
Abstract
We have previously reported the presence of feline immunodeficiency vi rus (FIV)-specific, major histocompatibility complex (MHC)-restricted cytolytic T lymphocytes (CTL) in experimentally FIV-infected cats. How ever, the fine specificity of the CTL and the role of individual FIV p roteins in inducing FIV-specific CTL responses remain unknown. In this study, we examined the in vitro induction and activity of FIV p24 cap sid-specific CTL obtained from cats that had been experimentally infec ted with FIV Petalurna for 30 to 56 months. An amphotropic murine retr oviral vector was used to generate transgenic primary feline T lymphob lasts that expressed the FIV capsid protein. When the autologous capsi d-transduced T cells were used in vitro to stimulate CTL responses fro m peripheral blood mononuclear cells of chronically infected cats, MHC -restricted lysis of virus-infected target cells was observed. The maj ority of the CTL expressed CD8, and depletion of this population, but not CD4(+) cells, effectively diminished the CTL activity. When the au tologous capsid-transduced T cells were used as target cells, lysis by capsid-induced effecters was not observed. Analysis of capsid-transdu ced T cell clones revealed a variable and low level of capsid expressi on among the clones. This study demonstrates the potential for using r etroviral vectors as a means of inducing CTL effector cells that will specifically kill lentivirus-infected cells during lentiviral infectio n. (C) 1995 Academic Press, Inc.