Human immunodeficiency virus-specific T lymphocyte cell
Oxenius A., McLean AR., Fischer M., Price DA., Dawson SJ., Hafner R., Schneider C., Joller H., Hirschel B., Phillips RE., Weber R., Günthard HF., Battegay M., Bucher H., Bernasconi E., Piffaretti JC., Bürgisser P., Francioli P., Pantaleo G., Rickenbach M., Telenti A., Egger M., Erb P., Klimkait T., Fierz W., Vernazza P., Wagels T., Flepp M., Günthard H., Grob P., Ledergerber B., Lauper U., Opravil M., Speck R., Trkola A., Weber R., Furrer HJ., Gorgievski M., Kaiser L., Perrin L., Yerly S., Kind C., Paccaud F., Rudin C., Schüpbach J.
Recent developments in HIV-specific CTL quantification (staining with MHC-epitopic peptide tetramers and IFNγ production) have shed new light on human immunodeficiency virus (HIV)-specific cytotoxic T lymphocytes (CTL). One week after infection, anti-HIV CTLs quickly appear, with a weak specificity spectrum which broaden afterwards. During the asymptomatic stage, an equilibrum between host and virus exists, characterized by vigourous CTL responses (frequencies: 10-2to 10-3CD8 T cells) directed against all HIV proteins and poor HIV replication. The ratio anti-HIV CTL : CD4 infected cells is 10:1, thus in favour of CTL action. When HIV viral load rises up, Aids stage is reached due to either viral escape or immune system exhaustion. Highly active antiretroviral therapies permit some immune reconstitution while effector CTLs decrease. Even if it is controled. HIV is still present in « viral reservoir ».