CD8+-cell antiviral factors not restricted to cytotoxic T cells induced during HIV
15 June 2000. Related: Basic science and immunology.
T cells induced during HIV CD8+-cell antiviral factors are not restricted to HIV-specific CD8+ cells, according to a report published in the May issue of the Journal of Virology. The report implies, according to the researchers, that CD8+ T cells, regardless of specificity, contribute to this effect through cell antiviral factors that are present after T-cell receptor stimulation occurs.
Dr Yves Riviere, of the Institut Pasteur, in Paris, France, and colleagues demonstrated that, using an HIV Nef-specific cytotoxic-T-lymphocyte (CTL) line and autologous CD4+ T cells infected with a nef-deleted HIV-1 virus, viral suppression did ‘not require the presence of the specific antigen during the effector phase.’
The group also used an Epstein-Barr virus (EBV)-specific cytotoxic T-lymphocyte line from an HIV-negative subject to show that ‘the ability to inhibit HIV replication in a noncytolytic manner is not restricted to HIV-specific effector cells.’ They found that EBV-specific CTL were as effective as ‘HIV-specific effectors in suppressing R5 or X4 HIV-1 strain replication in vitro.’
In addition, Dr Riviere’s team found that HIV suppressive activity was ‘detectable for up to 14 days following stimulation of EBV-specific CD8+ cells with the cognate epitope peptide.’
The group also reports that after infection of ‘CEM cells with an X4 strain of HIV-1, EBV-specific CTL line supernatant containing HIV-suppressive activity did not block virus entry but was shown to interfere with virus replication after the first template switching of reverse transcription.’
The researchers suggest that in HIV infection the ‘production of antiviral soluble factors by CD8+ T cells could be of importance in the in vivo control of viral latency.’
T cells induced during HIV CD8+-cell antiviral factors are not restricted to HIV-specific CD8+ cells, according to a report published in the May issue of the Journal of Virology. The report implies, according to the researchers, that CD8+ T cells, regardless of specificity, contribute to this effect through cell antiviral factors that are present after T-cell receptor stimulation occurs.
Dr Yves Riviere, of the Institut Pasteur, in Paris, France, and colleagues demonstrated that, using an HIV Nef-specific cytotoxic-T-lymphocyte (CTL) line and autologous CD4+ T cells infected with a nef-deleted HIV-1 virus, viral suppression did ‘not require the presence of the specific antigen during the effector phase.’
The group also used an Epstein-Barr virus (EBV)-specific cytotoxic T-lymphocyte line from an HIV-negative subject to show that ‘the ability to inhibit HIV replication in a noncytolytic manner is not restricted to HIV-specific effector cells.’ They found that EBV-specific CTL were as effective as ‘HIV-specific effectors in suppressing R5 or X4 HIV-1 strain replication in vitro.’
In addition, Dr Riviere’s team found that HIV suppressive activity was ‘detectable for up to 14 days following stimulation of EBV-specific CD8+ cells with the cognate epitope peptide.’
The group also reports that after infection of ‘CEM cells with an X4 strain of HIV-1, EBV-specific CTL line supernatant containing HIV-suppressive activity did not block virus entry but was shown to interfere with virus replication after the first template switching of reverse transcription.’
The researchers suggest that in HIV infection the ‘production of antiviral soluble factors by CD8+ T cells could be of importance in the in vivo control of viral latency.’
Source: Reuters Health
Reference:
J Virol 2000;74:4456-4464.