Author(s): Holznagel E, Norley S, Holzammer S, Coulibaly C, Kurth R
Abstract Share this page
Abstract The African green monkey (AGM) model system for simian immunodeficiency virus (SIV(agm)) has been used to examine why prolonged infection with the relevant virus does not result in the development of immunodeficiency in its natural host. Blood lymphocyte subset values were determined in uninfected (n=88) and naturally SIV(agm)-infected AGMs (n=74). A number of blood cell subsets, such as CD8alpha(+)CD3(+)CD28(neg), CD8alpha(+)CD3(neg) and CD20(+) cells, were expanded significantly in clinically asymptomatic animals carrying a relatively high plasma load of viral RNA (10(4)-10(7) RNA copies/ml plasma). The expanded CD8alpha(+)CD3(+)CD28(neg) subpopulation (1094 +/- 986 cells/microl blood in infected animals versus 402 +/- 364 cells/microl blood, P=0.03) comprised cells that resembled terminally differentiated effector CD8 T cells (CD27(neg) and CD11a(+)). In SIV(agm)-infected animals, the expanded CD8alpha(+)CD3(neg) cell subset shared identity with the CD16(+) population (natural killer cells). These results demonstrate for the first time that apathogenic SIV(agm) infection causes significant changes in the immune system of its natural host. Although previous studies had indicated that noncytotoxic mechanisms might play an important role in the suppression of virus replication in the natural host of SIV(agm), this study sheds new light on the possible role of cytotoxic T lymphocytes, the innate immune system and double-positive T helper cells (CD4(+)CD8alpha(+)CD3(+)) in suppressing virus replication in this animal model of AIDS.
This article was published in J Gen Virol
and referenced in Epidemiology: Open Access