Open AccessInhibition of cellular activation of retroviral replication by CD8 + T cells derived from non‐human primates
Author(s) -
POWELL J. D.,
BEDNARIK D. P.,
FOLKS T. M.,
JEHUDACOHEN T.,
VILLINGER F.,
SELL K. W.,
ANSARI A. A.
Publication year - 1993
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1993.tb05927.x
Subject(s) - biology , immunology , virology , replication (statistics) , cytotoxic t cell , cd8 , viral replication , genetics , immune system , virus , in vitro
SUMMARY To test the hypothesis that CD8 + T cells inhibit viral replication at the level of cellular activation, an Epstein‐Barr virus (EBV)‐transformed cell line (FEcl) from a simian immunodeficiency virus (SIV)‐seropositive sooty mangabey monkey was transfected with a human CD4 gene and shown to be replication‐competent for HIV‐1, HIV‐2 and SIV. Utilizing a dual‐chamber culture system, it was found that inhibition of viral replication can be mediated by a soluble factor. The FEcl cell line was transiently transfected with an LTR‐driven CAT reporter gene. It was found that autologous CD8 + T cells markedly inhibited CAT activity. Furthermore, co‐transfection of the FEcl cell line with an LTR‐driven tat plasmid and LTR‐CAT was able to quantitatively mitigate the suppressive effect. Thus, this inhibition appears to be directed at cellular mechanisms of viral transcription. Control transfections with an LTR‐driven CAT plasmid with a mutation at the NFkB binding site yielded no CAT activity, suggesting that most viral replication as measured by CAT activity is dependent, to a large extent, upon cellularly derived NFkB binding proteins.